Complement Activation: The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.Complement C3: A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.Complement System Proteins: Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).Complement C4: A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.Complement Pathway, Alternative: Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Complement Membrane Attack Complex: A product of COMPLEMENT ACTIVATION cascade, regardless of the pathways, that forms transmembrane channels causing disruption of the target CELL MEMBRANE and cell lysis. It is formed by the sequential assembly of terminal complement components (COMPLEMENT C5B; COMPLEMENT C6; COMPLEMENT C7; COMPLEMENT C8; and COMPLEMENT C9) into the target membrane. The resultant C5b-8-poly-C9 is the "membrane attack complex" or MAC.Complement Pathway, Classical: Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Blood Proteins: Proteins that are present in blood serum, including SERUM ALBUMIN; BLOOD COAGULATION FACTORS; and many other types of proteins.Anesthesia, Epidural: Procedure in which an anesthetic is injected into the epidural space.Plasma Substitutes: Any liquid used to replace blood plasma, usually a saline solution, often with serum albumins, dextrans or other preparations. These substances do not enhance the oxygen- carrying capacity of blood, but merely replace the volume. They are also used to treat dehydration.Dextrans: A group of glucose polymers made by certain bacteria. Dextrans are used therapeutically as plasma volume expanders and anticoagulants. They are also commonly used in biological experimentation and in industry for a wide variety of purposes.Meperidine: A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.Arthroplasty, Replacement, Hip: Replacement of the hip joint.Bupivacaine: A widely used local anesthetic agent.Properdin: A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections.ArchivesBiological Science Disciplines: All of the divisions of the natural sciences dealing with the various aspects of the phenomena of life and vital processes. The concept includes anatomy and physiology, biochemistry and biophysics, and the biology of animals, plants, and microorganisms. It should be differentiated from BIOLOGY, one of its subdivisions, concerned specifically with the origin and life processes of living organisms.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Directories as Topic: Lists of persons or organizations, systematically arranged, usually in alphabetic or classed order, giving address, affiliations, etc., for individuals, and giving address, officers, functions, and similar data for organizations. (ALA Glossary of Library and Information Science, 1983)Chlamydophila pneumoniae: A species of CHLAMYDOPHILA that causes acute respiratory infection, especially atypical pneumonia, in humans, horses, and koalas.Basophil Degranulation Test: An in vitro test used in the diagnosis of allergies including drug hypersensitivity. The allergen is added to the patient's white blood cells and the subsequent histamine release is measured.Haptens: Small antigenic determinants capable of eliciting an immune response only when coupled to a carrier. Haptens bind to antibodies but by themselves cannot elicit an antibody response.Immunoglobulin Constant Regions: The domains of the immunoglobulin molecules that are invariable in their amino acid sequence within any class or subclass of immunoglobulin. They confer biological as well as structural functions to immunoglobulins. One each on both the light chains and the heavy chains comprises the C-terminus half of the IMMUNOGLOBULIN FAB FRAGMENT and two or three of them make up the rest of the heavy chains (all of the IMMUNOGLOBULIN FC FRAGMENT)Mannose-Binding Lectin: A specific mannose-binding member of the collectin family of lectins. It binds to carbohydrate groups on invading pathogens and plays a key role in the MANNOSE-BINDING LECTIN COMPLEMENT PATHWAY.Complement Pathway, Mannose-Binding Lectin: Complement activation triggered by the interaction of microbial POLYSACCHARIDES with serum MANNOSE-BINDING LECTIN resulting in the activation of MANNOSE-BINDING PROTEIN-ASSOCIATED SERINE PROTEASES. As in the classical pathway, MASPs cleave COMPLEMENT C4 and COMPLEMENT C2 to form C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.Mannose-Binding Protein-Associated Serine Proteases: Serum serine proteases which participate in COMPLEMENT ACTIVATION. They are activated when complexed with the MANNOSE-BINDING LECTIN, therefore also known as Mannose-binding protein-Associated Serine Proteases (MASPs). They cleave COMPLEMENT C4 and COMPLEMENT C2 to form C4b2a, the CLASSICAL PATHWAY C3 CONVERTASE.Collectins: A class of C-type lectins that target the carbohydrate structures found on invading pathogens. Binding of collectins to microorganisms results in their agglutination and enhanced clearance. Collectins form trimers that may assemble into larger oligomers. Each collectin polypeptide chain consists of four regions: a relatively short N-terminal region, a collagen-like region, an alpha-helical coiled-coil region, and carbohydrate-binding region.Reperfusion Injury: Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.Physiological Phenomena: The functions and properties of living organisms, including both the physical and chemical factors and processes, supporting life in single- or multi-cell organisms from their origin through the progression of life.Metabolic Networks and Pathways: Complex sets of enzymatic reactions connected to each other via their product and substrate metabolites.British Columbia: A province of Canada on the Pacific coast. Its capital is Victoria. The name given in 1858 derives from the Columbia River which was named by the American captain Robert Gray for his ship Columbia which in turn was named for Columbus. (From Webster's New Geographical Dictionary, 1988, p178 & Room, Brewer's Dictionary of Names, 1992, p81-2)Academies and Institutes: Organizations representing specialized fields which are accepted as authoritative; may be non-governmental, university or an independent research organization, e.g., National Academy of Sciences, Brookings Institution, etc.Systems Biology: Comprehensive, methodical analysis of complex biological systems by monitoring responses to perturbations of biological processes. Large scale, computerized collection and analysis of the data are used to develop and test models of biological systems.Animal Testing Alternatives: Procedures, such as TISSUE CULTURE TECHNIQUES; mathematical models; etc., when used or advocated for use in place of the use of animals in research or diagnostic laboratories.Food, Genetically Modified: Food derived from genetically modified organisms (ORGANISMS, GENETICALLY MODIFIED).Carcinogenicity Tests: Tests to experimentally measure the tumor-producing/cancer cell-producing potency of an agent by administering the agent (e.g., benzanthracenes) and observing the quantity of tumors or the cell transformation developed over a given period of time. The carcinogenicity value is usually measured as milligrams of agent administered per tumor developed. Though this test differs from the DNA-repair and bacterial microsome MUTAGENICITY TESTS, researchers often attempt to correlate the finding of carcinogenicity values and mutagenicity values.Copyright: It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)Pathology, Clinical: A subspecialty of pathology applied to the solution of clinical problems, especially the use of laboratory methods in clinical diagnosis. (Dorland, 28th ed.)Complement C1q: A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.Lung Neoplasms: Tumors or cancer of the LUNG.Yucca: A genus (and common name) in the AGAVACEAE family. It is known for SAPONINS in the root that are used in SOAPS.Alexander Disease: Rare leukoencephalopathy with infantile-onset accumulation of Rosenthal fibers in the subpial, periventricular, and subependymal zones of the brain. Rosenthal fibers are GLIAL FIBRILLARY ACIDIC PROTEIN aggregates found in ASTROCYTES. Juvenile- and adult-onset types show progressive atrophy of the lower brainstem instead. De novo mutations in the GFAP gene are associated with the disease with propensity for paternal inheritance.Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.Nodal Signaling Ligands: Members of the transforming growth factor superfamily that play a role in pattern formation and differentiation during the pregastrulation and GASTRULATION stages of chordate development. Several nodal signaling ligands are specifically involved in the genesis of left-right asymmetry during development. The protein group is named after a critical region of the vertebrate embryo PRIMITIVE STREAK referred to as HENSEN'S NODE.Carcinoma, Non-Small-Cell Lung: A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.Heparan Sulfate Proteoglycans: Ubiquitous macromolecules associated with the cell surface and extracellular matrix of a wide range of cells of vertebrate and invertebrate tissues. They are essential cofactors in cell-matrix adhesion processes, in cell-cell recognition systems, and in receptor-growth factor interactions. (From Cancer Metastasis Rev 1996; 15(2): 177-86; Hepatology 1996; 24(3): 524-32)Complement C3b: The larger fragment generated from the cleavage of COMPLEMENT C3 by C3 CONVERTASE. It is a constituent of the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb), and COMPLEMENT C5 CONVERTASES in both the classical (C4b2a3b) and the alternative (C3bBb3b) pathway. C3b participates in IMMUNE ADHERENCE REACTION and enhances PHAGOCYTOSIS. It can be inactivated (iC3b) or cleaved by various proteases to yield fragments such as COMPLEMENT C3C; COMPLEMENT C3D; C3e; C3f; and C3g.Heparitin Sulfate: A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.Complement Inactivator Proteins: Serum proteins that negatively regulate the cascade process of COMPLEMENT ACTIVATION. Uncontrolled complement activation and resulting cell lysis is potentially dangerous for the host. The complement system is tightly regulated by inactivators that accelerate the decay of intermediates and certain cell surface receptors.

Up-regulated production and activation of the complement system in Alzheimer's disease brain. (1/1999)

We used reverse transcriptase-polymerase chain reaction and Western blotting techniques to measure the levels of complement mRNAs and their protein products in Alzheimer's disease (AD) brain compared with non-AD brain. mRNAs for C1q, C1r, C1s, C2, C3, C4, C5, C6, C7, C8, and C9 were detected in the 11 regions of brain that were investigated. The mRNA levels were markedly up-regulated in affected areas of AD brain. In the entorhinal cortex, hippocampus, and midtemporal gyrus, which had dense accumulations of plaques and tangles, C1q mRNA was increased 11- to 80-fold over control levels, and C9 mRNA 10- to 27-fold. These levels were substantially higher than in the livers of the same cases. Western blot analysis of AD hippocampus established the presence of all of the native complement proteins as well as their activation products C4d, C3d, and the membrane attack complex. These data indicate that high levels of complement are being produced in affected areas of AD brain, that full activation of the classical complement pathway is continuously taking place, and that this activation may be contributing significantly to AD pathology.  (+info)

Capsular sialic acid limits C5a production on type III group B streptococci. (2/1999)

The majority of type III group B streptococcus (GBS) human neonatal infections are caused by a genetically related subgroup called III-3. We have proposed that a bacterial enzyme, C5a-ase, contributes to the pathogenesis of neonatal infections with GBS by rapidly inactivating C5a, a potent pro-inflammatory molecule, but many III-3 strains do not express C5a-ase. The amount of C5a produced in serum following incubation with representative type III strains was quantitated in order to better understand the relationship between C5a production and C5a-ase expression. C5a production following incubation of bacteria with serum depleted of antibody to the bacterial surface was inversely proportional to the sialic acid content of the bacterial capsule, with the more heavily sialylated III-3 strains generating less C5a than the less-virulent, less-sialylated III-2 strains. The amount of C5a produced correlated significantly with C3 deposition on each bacterial strain. Repletion with type-specific antibody caused increased C3b deposition and C5a production through alternative pathway activation, but C5a was functionally inactivated by strains that expressed C5a-ase. The increased virulence of III-3 strains compared to that of III-2 strains results at least partially from the higher sialic acid content of III-3 strains, which inhibits both opsonophagocytic killing and C5a production in the absence of type-specific antibody. We propose that C5a-ase is not necessary for III-3 strains to cause invasive disease because the high sialic acid content of III-3 strains inhibits C5a production.  (+info)

Polymerization of IgA and IgM: roles of Cys309/Cys414 and the secretory tailpiece. (3/1999)

We have investigated how the secretory tailpiece (tp), Cys414 and the amino acids flanking Cys414 or Cys309 are involved in regulating the different polymerization of IgM and IgA to pentamers and dimers/monomers, respectively. Whereas changing the tp of IgM to that of IgA has little effect on IgM polymerization, introducing the mu tp to IgA leads to the formation of larger than wild-type IgA polymers, including pentamers and hexamer. This shows that the secretory tp can differentially regulate polymerization depending on the heavy chain context. Cys414, which is engaged in intermonomeric disulfide bonds in IgM, is not crucial for the difference in IgM and IgA polymerization; IgM with a C414S mutation forms more large polymers than IgA. Also, IgA with IgM-like mutations in the five amino acids flanking Cys309, which is homologous to Cys414, oligomerize similarly as IgA wild type. Thus, IgA appears to have an inherent tendency to form monomers and dimers that is partially regulated by the tp, while the Cys309 region has only a minor effect. We also show that complement activation by IgM is sensitive to alterations in the polymeric structure, while IgA is inactive in classical complement activation even for polymers such as pentamers and hexamers.  (+info)

Two constituents of the initiation complex of the mannan-binding lectin activation pathway of complement are encoded by a single structural gene. (4/1999)

Mannan-binding lectin (MBL) forms a multimolecular complex with at least two MBL-associated serine proteases, MASP-1 and MASP-2. This complex initiates the MBL pathway of complement activation by binding to carbohydrate structures present on bacteria, yeast, and viruses. MASP-1 and MASP-2 are composed of modular structural motifs similar to those of the C1q-associated serine proteases C1r and C1s. Another protein of 19 kDa with the same N-terminal sequence as the 76-kDa MASP-2 protein is consistently detected as part of the MBL/MASP complex. In this study, we present the primary structure of this novel MBL-associated plasma protein of 19 kDa, MAp19, and demonstrate that MAp19 and MASP-2 are encoded by two different mRNA species generated by alternative splicing/polyadenylation from one structural gene.  (+info)

Role of antibody and complement in opsonization of group B streptococci. (5/1999)

A requirement for the classic complement pathway in opsonization of group B streptococci was observed by using both a chemiluminescence and a radiolabeled bacterial uptake technique. The classic pathway increased levels of opsonization for types Ia and II stock and wild strains and for some type III wild strains. In contrast, other type III wild strains and the type III stock strain had accelerated kinetics of uptake in the presence of an intact classic pathway, but the level of opsonization was unchanged from that with antibody alone. We could not demonstrate a significant role for the alternative pathway in opsonizing stock or wild strains of group B streptococci. Futhermore, electrophoretic and complement consumption analysis by hemolytic titration failed to reveal alternative pathway activation by the majority of strains of this group. Therapy aimed at supplying opsonins for these organisms will require the presence of type-specific antibody.  (+info)

Anti-endothelial cell antibodies in systemic vasculitis and systemic lupus erythematosus (SLE): effects of heat inactivation on binding and specificity. (6/1999)

Heating sera is used to inactivate complement but may affect the binding characteristics of autoantibodies. We studied the effect of heating sera from patients with systemic vasculitides and SLE on antibody binding to cultured human umbilical vein endothelial cells. Sera from 32 patients with systemic vasculitides, eight with SLE and 10 healthy controls were studied for anti-endothelial cell antibodies (AECA) using an ELISA before and after heating sera to 56 degrees C for 30 min. The median (range) AECA binding index in the patient group increased from 20% (0-153%) to 71.5% (10-259%) (P < 0.0001). The AECA binding index in the control group also increased from 14% (0-52%) to 90% (42-154%) (P < 0.0001). The increased binding was unaffected by the addition of fresh complement or removal of immune complexes and the increased binding after heating persisted even after cooling to 4 degrees C. Specificity experiments showed that after heating, the binding specificity of sera was lost. Removal of immunoglobulin with Protein A abolished the increased binding seen after heating. Heating sera increases AECA binding in both patient and control sera. The mechanism is probably non-specific damage to the immunoglobulin molecule, and heating sera should thus be avoided.  (+info)

Influence of dialysis with polyamide vs haemophan haemodialysers on monokines and complement activation during a 4-month long-term study. (7/1999)

BACKGROUND: Contact between blood and dialysis membranes activates mononuclear cells and the complement system. The extent of activation is dependent on the dialyser material used and is considered an index of biocompatibility. Polyamide dialysers consist of a synthetic membrane that claims high standards of biocompatibility. Haemophan dialysers represent membranes made of modified cellulose that are now broadly used for treatment in Europe and are already considered to be more biocompatible than the cuprophane membranes that were used as reference in most previous studies. METHODS: In a cross-over treatment study short-term as well as long-term effects of a polyamide dialyser with respect to monokine induction and complement activation were compared to a haemophan dialyser. RESULTS: Neither haemophan nor polyamide dialysers induced relevant changes in plasma monokine levels. However, in vitro challenge of mononuclear cells with lipopolysaccharide (LPS) unmasked a significantly stronger preactivation for the secretion of proinflammatory monokines during haemophan than polyamide dialysis. Unlike other monokines the production of the regulatory monokine IL-10 was mainly influenced by individual factors and correlated with the patient's immune status rather than the dialyser type used. Enhanced preactivation of monocytes in haemophan compared to polyamide dialysis was paralleled by an increased complement activation. Cellular preactivation and formation of terminal complement complex remained constant over the 4-month treatment period. CONCLUSIONS: Haemophan and polyamide dialysers do not induce changes in plasma cytokine levels both during short-term and long-term use. However, they significantly differ in complement activation as well as preactivation of monocytes. Preactivated monocytes are prone to secrete high amounts of proinflammatory cytokines when exposed to a second stimulus like endotoxin. Secretion of the regulatory cytokine IL-10 is not influenced by the dialyser type.  (+info)

Recombinant glycoproteins that inhibit complement activation and also bind the selectin adhesion molecules. (8/1999)

Soluble human complement receptor type 1 (sCR1, TP10) has been expressed in Chinese hamster ovary (CHO) DUKX-B11 cells and shown to inhibit the classical and alternative complement pathways in vitro and in vivo. A truncated version of sCR1 lacking the long homologous repeat-A domain (LHR-A) containing the C4b binding site has similarly been expressed and designated sCR1[desLHR-A]. sCR1[desLHR-A] was shown to be a selective inhibitor of the alternative complement pathway in vitro and to function in vivo. In this study, sCR1 and sCR1[desLHR-A] were expressed in CHO LEC11 cells with an active alpha(1,3)-fucosyltransferase, which makes possible the biosynthesis of the sialyl-Lewisx (sLex) tetrasaccharide (NeuNAcalpha2-3Galbeta1-4(Fucalpha1-3)GlcNAc) during post-translational glycosylation. The resulting glycoproteins, designated sCR1sLex and sCR1[desLHR-A]sLex, respectively, retained the complement regulatory activities of their DUKX B11 counterparts, which lack alpha(1-3)-fucose. Carbohydrate analysis of purified sCR1sLex and sCR1[desLHR-A]sLex indicated an average incorporation of 10 and 8 mol of sLex/mol of glycoprotein, respectively. sLex is a carbohydrate ligand for the selectin adhesion molecules. sCR1sLex was shown to specifically bind CHO cells expressing cell surface E-selectin. sCR1[desLHR-A]sLex inhibited the binding of the monocytic cell line U937 to human aortic endothelial cells, which had been activated with tumor necrosis factor-alpha to up-regulate the expression of E-selectin. sCR1sLex inhibited the binding of U937 cells to surface-adsorbed P-selectin-IgG. sCR1sLex and sCR1[desLHR-A]sLex have thus demonstrated both complement regulatory activity and the capacity to bind selectins and to inhibit selectin-mediated cell adhesion in vitro.  (+info)

*Antibody

Complement activation (fixation), in which antibodies that are latched onto a foreign cell encourage complement to attack it ... Activation of complement[edit]. Antibodies that bind to surface antigens (for example, on bacteria) will attract the first ... these phagocytes are attracted by certain complement molecules generated in the complement cascade. Second, some complement ... component of the complement cascade with their Fc region and initiate activation of the "classical" complement system.[30] This ...

*John Raymond Hobbs

16, 301-310 Versey, J.M.B., Slater, L., Hobbs, J.R. Activation of complement in relation to disease, (1975) J.Clin.Path. 28, ... Complement activation. Mixed lymphocyte reaction T-cell receptors. Phagocyte function. First to fully describe IgA deficiency. ... Target cell death without added complement after cooperation of 7S-antibodies with non-immune lymphocytes. (1972) Nature New ...

*FOXA3

Corrocher R, Tedesco F, Rabusin P, De Sandre G (1975). "Effect of human erythrocyte stromata on complement activation". Br. J. ... Lin B, Morris DW, Chou JY (1997). "The role of HNF1alpha, HNF3gamma, and cyclic AMP in glucose-6-phosphatase gene activation". ... "Analysis of hepatocyte nuclear factor-3 beta protein domains required for transcriptional activation and nuclear targeting" ...

*Lesional demyelinations of the central nervous system

There is no complement activation or MAG loss. The meaning of this fact is controversial. For some investigation teams it means ... but also signs of complement system activation can be found. Though this pattern could be considered similar to damage seen in ... but no signs of complement system activation. Pattern II The scar presents T-cells and macrophages around blood vessels, with ... which was associated with internalization of AQP4 and AQP1 and astrocyte apoptosis in the absence of complement activation. ...

*Kolektin - Wikipedie

Watford WT, Wright JR, Hester CG, Jiang H, Frank MM (2001). "Surfactant Protein A Regulates Complement Activation". J Immunol ... Watford WT, Ghio AJ, Wright JR (2000). "Complement-mediated host defense in the lung". Am J Physiol Lung Cell Mol Physiol 279: ... Alvarez-Dominguez C, Carrasco-Marin E, Leyva-Cobian F (1993). "Role of Complement Component Clq in Phagocytosis of Listeria ... Selander B, Mårtensson U, Weintraub A (2006). "Mannan-binding lectin activates C3 and the alternative complement pathway ...

*Humoral immunity

The classical complement pathway typically requires antibodies for activation and is a specific immune response, while the ... Complement system[edit]. Main article: Complement system. The complement system is a biochemical cascade of the innate immune ... Three biochemical pathways activate the complement system: the classical complement pathway, the alternate complement pathway, ... classical complement activation, and opsonin promotion of phagocytosis and pathogen elimination.[1] ...

*Xenotransplantation

The binding of XNAs initiate complement activation through the classical complement pathway. Complement activation causes a ... Interruption of the complement cascade *The recipient's complement cascade can be inhibited through the use of cobra venom ... Expression of human complement regulators (CD55, CD46, and CD59) to inhibit the complement cascade.[27] ... complement pathway activation and delayed type hypersensitivity (DTH).. Acute vascular rejection[edit]. Also known as delayed ...

*Sialic acid

This prevents activation of complement. Sialic acid in the form of polysialic acid is an unusual posttranslational modification ...

*ABCB5

Corrocher R, Tedesco F, Rabusin P, De Sandre G (February 1975). "Effect of human erythrocyte stromata on complement activation ... "Modulation of T-cell activation by malignant melanoma initiating cells". Cancer Research. 70 (2): 697-708. doi:10.1158/0008- ...

*C3-convertase

Hourcade D, Holers VM, Atkinson JP (1989). "The regulators of complement activation (RCA) gene cluster". Adv Immunol. Advances ... Properdin (Factor P) is the only known positive regulator of complement activation that stabilizes the alternative C3 ... "Formation of classical C3 convertase during the alternative pathway of human complement activation". PubMed Article. Retrieved ... C3 convertase (EC 3.4.21.43, C42 , C4bC2b, C3bBb, complement C.hivin.4.hivin2, complement C3 convertase) belongs to family of ...

*Pathology of multiple sclerosis

There is no complement activation or MAG loss. These differences are noticeable only in early lesions and the heterogeneity was ... but also signs of complement system activation can be found. This pattern has been considered similar to damage seen in NMO, ... but no signs of complement system activation. Pattern II The scar presents T-cells and macrophages around blood vessels, with ... Complement C3 on microglial clusters in multiple sclerosis occur in chronic but not acute disease: Implication for disease ...

*Chemorepulsion

Increased expression of surface molecules that inhibit complement activation. Local production of immunosuppressive cytokines, ... 2001). "Activation of RhoA and ROCK are essential for detachment of migrating leukocytes". Mol. Biol. Cell. 12 (7): 2137-2145. ... The chemorepellent 8CPT-cAMP inhibits PLC activity and thereby increases Ptds(3,4,5)P3 accumulation and activation of PTEN. In ... Kotwal, GJ (2000). "Poxviral mimicry of complement and chemokine system components: what's the end game?". Immunol Today. 21 (5 ...

*Antileukotriene

"Evid Based Complement Alternat Med. 2014: 960258. doi:10.1155/2014/960258. PMC 4058220. PMID 24976853. These researches are ... Frieri M (2015). "Mast Cell Activation Syndrome". Clin Rev Allergy Immunol. doi:10.1007/s12016-015-8487-6. PMID 25944644.. ... 1999), in which hyperforin provided a potent inhibition of TNFα-induced activation of NF-κB [58]. Another important activity ...

*Cutaneous small-vessel vasculitis

... immune complexes deposit in vessel walls leading to activation of the complement system. C3a and C5a, proteins produced from ... the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, ...

*Guillain-Barré syndrome

... this process is preceded by activation of a group of blood proteins known as complement. In contrast, the axonal variant is ... Given the role of the complement system in GBS, it has been suggested that complement inhibitors (such as the drug eculizumab) ... mediated by IgG antibodies and complement against the cell membrane covering the axon without direct lymphocyte involvement.[8] ...

*C1 complex

Activation of the C1 complex initiates the classical complement pathway. This occurs when C1q binds to antigen-antibody ... Deciphering the fine details of C1 assembly and activation mechanisms: "mission impossible"? Complement C1 at the US National ... The C1 complex (complement component 1, C1) is a protein complex involved in the complement system. It is the first component ... 2001). "The complement system and innate immunity". Immunobiology: The Immune System in Health and Disease. New York: Garland ...

*Liver transplantation

Complement activation is involved and the effect is usually profound. Hyperacute rejection happens within minutes to hours ...

*FCN3

Matsushita M, Kuraya M, Hamasaki N (2002). "Activation of the lectin complement pathway by H-ficolin (Hakata antigen)". J. ... The protein can activate the complement pathway in association with MASPs and sMAP, thereby aiding in host defense through the ... activation of the lectin pathway. Alternative splicing occurs at this locus and two variants, each encoding a distinct isoform ...

*Autoimmune hemolytic anemia

Antibodies are produced against the RBCs, which leads to complement activation. Complement fragments, such as C3a, C4a and C5a ... Warm-type AIHA shows a positive reaction with antisera to IgG antibodies with or without complement activation. Cases may also ... In order for intravascular AIHA to be recognizable, it requires overwhelming complement activation, therefore most AIHA is ... IgM is a potent activator of the classical complement pathway, thus, AIHA involving IgM is characterized by complement mediated ...

*Antibody-dependent enhancement

The infection of HIV-1 leads to activation of complements fragments of these complements can assist viruses with infection by ... ISBN 1-55581-393-3. Yu, Q; Yu, R; Qin, X (2010). "The good and evil of complement activation in HIV-1 infection". Cellular and ... Complement Component receptors CR2, CR3 and CR4 have been found to mediate this Complement -Mediated enhancement of infection. ... ADE in HIV can be complement mediated or Fc receptor mediated. Complements in presence of HIV-1 positive sera have been found ...

*Collectin

... s are linked with activation of lectin pathway of complement activation. At the beginning, there is a binding of ... complement activation, opsonization, activation of phagocytosis, or inhibition of microbial growth. Other functions of ... Collectin MBL is involved in activation of the lectin complement pathway. There are three serine proteases, MASP-1, 2 and 3 ( ... MBL can bind to microorganisms and this interaction can lead to opsonization through complement activation, or it can opsonize ...

*Adaptive immune system

One set of innate immune mechanisms is humoral, such as complement activation. Another set comprises pattern recognition ... Clustered Band 3 proteins with attached antibodies activate complement, and complement C3 fragments are opsonins recognized by ... Reduces number of infectious units to be dealt with Activation of complement: Cause inflammation and cell lysis Opsonization: ... CTL activation is tightly controlled and in general requires a very strong MHC/antigen activation signal, or additional ...

*Glutamyl endopeptidase GluV8

Glutamyl endopeptidase can inhibit the activation of targets within the complement system. It is indicated to cause inhibition ... to all three pathways of complement activation. Glutamyl endopeptidase can furthermore cleave a wide array bacterial surface ... Nickerson, Nicholas N.; Prasad, Lata; Jacob, Latha; Delbaere, Louis T.; McGavin, Martin J. (2007-11-23). "Activation of the ... precursor activation mechanisms reveals unique secretion kinetics of proSspB (Staphopain B), and a different interaction with ...

*J chain

The J-chain also plays a role in the activation of complement. J-chain negative IgM hexamers are 15-20 times more effective at ... A consequence of this lack of complement activation is it allows J-chain positive pIgM to bind antigens without causing ... excessive damage to epithelial membranes through complement activation. GRCh38: Ensembl release 89: ENSG00000132465 - Ensembl, ... activating complement than J-chain positive IgM pentamers. ...

*MASP1 (protein)

This protein is not directly involved in complement activation but may play a role as an amplifier of complement activation by ... MASP-1 is a serine protease that functions as a component of the lectin pathway of complement activation. The complement ... Petersen SV, Thiel S, Jensenius JC (Aug 2001). "The mannan-binding lectin pathway of complement activation: biology and disease ... with pattern recognition molecules of the complement system and regulating the lectin pathway of complement activation". ...

*Plasma cell

These T cells bind to the MHC II-antigen molecule and cause activation of the B cell. This is a type of safeguard to the system ... the activation and growth of B cell clones able to secrete antibodies of higher affinity for the antigen. ... Immunology: lymphocytic adaptive immune system and complement. Lymphoid. Antigens. *Antigen *Superantigen. *Allergen ...
Purpose The purpose of this study was to investigate complement activation and associated inflammatory mechanisms in normal, aged human retina. in the choriocapillaris, and in BM. Lectin binding of RCA-I was Rabbit polyclonal to CREB1 strong throughout the neuroretina. Conclusions Robust immunostaining for APP in older donor eyes suggested that amyloid beta peptides may be one of the triggers of complement activation during the normal aging process. Microglial markers CD11b and RCA-I also increase with age, suggesting a concomitant inflammatory response to C5b-9 deposits in the retinal pigment epithelium, BM, and CC. Immunoreactivity for CD36 was strong in both age groups; the lack of age dependence in this candidate receptor for amyloid beta suggested that complement activation may arise from interactions of amyloid beta with other candidate receptors in normal human retina. Latest research have got supplied book understanding TSA cell signaling in to the function from the supplement system and ...
Ischemia and reperfusion of organs is an unavoidable consequence of transplantation. Inflammatory events associated with reperfusion injury are in part attributed to excessive complement activation. Systemic administration of complement inhibitors reduces reperfusion injury but leaves patients vulnerable to infection. Here, we report a novel therapeutic strategy that decorates cells with an anti-complement peptide. An analog of the C3 convertase inhibitor Compstatin (C) was synthesized with a hexahistidine (His6) tag to create C-His6. To decorate cell membranes with C-His6, fusogenic lipid vesicles (FLVs) were used to incorporate lipids with nickel (Ni2+) tethers into cell membranes, and these could then couple with C-His6. Ni2+ tether levels to display C-His6 were modulated by changing FLV formulation, FLV incubation time and FLV levels. SKOV-3 cells decorated with C-His6 effectively reduced complement deposition in a classical complement activation assay. We conclude that our therapeutic ...
Activation of the complement cascade is clearly implicated in the pathology of multiple sclerosis (MS). However, the extent and nature of its involvement in specific athological processes remains uncertain. We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive MS, examining 35 different plaques, and 16 control donors, including 9 with CNS disease. Plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, TCC) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite no other evidence of on-going inflammation. Complement immunolabelling was most apparent in plaque and peri-plaque areas but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. Cellular ...
The present invention provides modified IgG3 containing human constant regions which has a shorter total-hinge region compared with normal human IgG3. Also described is a method for assaying an antibody against a specific antigen or hapten for its effectiveness in complement activation in an animal species, wherein the antibody is contacted with the immobilized antigen or hapten to form an immobilized antibody/antigen or hapten complex which is then contacted with complement from the relevant animal species, followed by assay of components of the complement complex thereby formed; whereby the extent and nature of complement activation by the antibody in the sample may be determined.
Purpose: Complement activation and oxidative stress have been increasingly implicated in the pathogenesis of AMD. Complement activation products have been detected in Bruchs membrane and drusen from patients, indicating that in AMD, complement attack likely occurs primarily on the RPE basal surface. Herein, we describe a model used to investigate the effect of oxidative stress on complement-mediated RPE cell injury, whereby complement attack was initiated with an RPE-specific priming antibody on the basal surface of differentiated human RPE cells.. Methods: ARPE-19 cells and RPE cells from 2 donors were cultured for one month on collagen-coated porous supports in DMEM-F12 containing 1% FBS. Transepithelial resistance (TER) was recorded, apical microvilli and tight junctions were identified by transmission electron microscope, and ZO-1 was examined by immuno-fluorescent staining. Cytokeratin-18 staining was used to confirm the epithelial nature of RPE cells. The cells were basally exposed for 2 ...
The complement system provides a fundamental component of the body's immune response to invading microorganisms. This chapter highlights the various roles of the complement system in the orchestration of the immune response towards microbial infections, gives examples of microbial strategies to evade complement-mediated clearance, and discusses how acquired and inherited complement deficiencies may predispose an organism to infectious disease. Complement is activated by three pathways: the classical pathway, the alternative pathway, and the lectin pathway. The lectin pathway is activated by carbohydrate recognition molecules that bind to polysaccharide on the surface of a pathogen. Factor B, factor D, and properdin (factor P) are specific components of the alternative pathway of complement activation. The complement activation is tightly regulated by membrane-bound and fluid-phase regulatory components to avoid runaway activation of the enzymatic cascade that could lead to excess host tissue damage
Adsorption, Blood Proteins/*chemistry/immunology/*metabolism, Coated Materials; Biocompatible/*chemistry/*metabolism, Complement Activation/*physiology, Complement C3/immunology/*metabolism, Complement Pathway; Alternative/physiology, Humans, Materials Testing, Polystyrenes/*chemistry, Protein Binding, Surface Properties ...
A Novel Protocol Allowing Oral Delivery of a Protein Complement Inhibitor that Subsequently Targets to Inflamed Colon Mucosa and Ameliorates Murine Colitis. Elvington, M; Blichmann, P; Qiao, F; Scheiber, M; Wadsworth, C; et al. A novel protocol allowing oral delivery of a protein complement inhibitor that subsequently targets to inflamed colon mucosa and ameliorates murine colitis. Clinical and Experimental Immunology 177.2 (Aug 2014): 500-508. While there is evidence of a pathogenic role for complement in inflammatory bowel disease, there is also evidence for a protective role that relates to host defence and protection from endotoxaemia. There is thus concern regarding the use of systemic complement inhibition as a therapeutic strategy. Local delivery of a complement inhibitor to the colon by oral administration would ameliorate such concerns, but while formulations exist for oral delivery of low molecular weight drugs to the colon, they have not been used successfully for oral delivery of ...
Learn how uncontrolled or excessive complement activation may play a role in several autoimmune and inflammatory diseases, and why APL-2 (pegcetacoplan) targeting of complement proteins at the level of C3 is being investigated as a treatment.
AMYNDAS is developing a novel peptidic complement inhibitor AMY-101, based on the third-generation compstatin analogue Cp40. AMY-101 is a selective inhibitor of complement activation in humans and in NHP. It binds to the complement component C3, the central functional hub that controls the upstream activation/amplification and downstream effector functions of complement. By binding to C3, AMY-101 inhibits the cleavage of native C3 to its active fragments C3a and C3b. As a consequence, the deposition of C3b, amplification via the alternative pathway and all downstream complement responses are prevented. AMY-101 is being developed to treat complement-mediated diseases, which are largely driven by aberrant C3 activation.. This first-in-human study of the C3-targeting complement inhibitor AMY-101 investigates the safety and PK/PD profile of AMY-101 in healthy male volunteers after Single Ascending Dose (SAD) and Multiple Doses (MD) using subcutaneous (SQ) or intravenous (IV) administration. The ...
Each pathway follows a sequence of reactions to generate a protease called a C3 convertase. The active protease is retained at the pathogen surface, and this ensures that the next complement zymogen in the pathway is also cleaved and activated at the pathogen surface. By contrast, the small peptide fragment is released from the site of the reaction and can act as a soluble mediator.. The early events of all three pathways of complement activation involve a series of cleavage reactions that culminate in the formation of an enzymatic activity called a C3 convertase, more The C3 convertases formed by these early events of complement activation are bound covalently to the pathogen surface. Here they cleave C3 to generate large amounts of C3bthe main effector molecule of the complement system, and C3a, a peptide mediator of inflammation.. The C3b molecules act as opsonins; they bind covalently to the pathogen and thereby target it for destruction by phagocytes equipped with receptors for C3b. These ...
The complement system is a biochemical cascade that helps, or complements, the ability of antibodies to clear pathogens from an organism. It is part of the immune system called the innate immune system that is not adaptable and does not change over the course of an individuals lifetime. However, it can be recruited and brought into action by the adaptive immune system. The Classical pathway of activation of the complement system is a group of blood proteins that mediate the specific antibody response. [source: Wikipedia] The Classical Pathway begins with circulating C1Q binding to an antigen on the surface of a pathogen, which goes on to active and recruit 2 copies of each C1R and C1S, forming a C1 complex. The activated C1 complex cleaves C2 and C4. Activated cleavage products C2A and C4B combine to form C3 convertase, which cleaves C3. The cleavage product C3B joins the complex to form C5 convertase, which cleaves C5. The cleavage product C5B joins C6, C7, C8 and multiple copies of C9 to form ...
Concerns that the immune system is a two-edged sword that sometimes inhibits and sometimes enhances tumor growth have focused on both the B-cell and T-cell arms of the immune system for over 40 years. While the clinical value of adoptively transfused T cells in a variety of clinical settings is well established (28), recent concerns have focused on regulatory mechanisms able to diminish the antitumor T-cell response and even enhance tumor growth (29). Antibodies and the B-cell response have long been associated with this dichotomy as well (30). Since FDA approval of mAbs such as Rituxan and Herceptin, and their widespread use, there is no doubt about the clinical value of immune effector mechanisms such as complement activation and antibody-dependant cellular cytotoxicity (ADCC), which these antibodies are known to mediate (8, 31). Despite the obvious value of adoptively administered antibodies and T cells, the role of vaccine-induced antibodies and T cells targeting cancer antigens remains less ...
Avhandlingar om COMPLEMENT ACTIVATION. Sök bland 90495 avhandlingar från svenska högskolor och universitet på Avhandlingar.se.
Antibodies of the IgG class can damage tissues in a variety of ways, including (i) directly through complement activation, (ii) indirectly through the deposition of immune complexes, and (iii) indirectly through the recruitment of cytotoxic or inflammation-inducing cells. Very high levels of antibody result in hyperacute rejection and graft failure, an outcome that can easily be avoided by the performance of a lymphocyte crossmatch test prior to transplantation. In contrast, clear elucidation of the relevance of donor-reactive antibodies of various strengths and specificities and of antibodies that arise after transplantation has been hampered by inadequate technologies and lack of reimbursement for posttransplant monitoring of antibodies. Nonetheless, a deleterious effect of antibody specific for mismatched donor HLA antigens has been demonstrated for nearly every type of organ and tissue that has been transplanted in sufficient numbers, including hematopoietic stem cells and, possibly, composite
The FARR assay identifies high avidity dsDNA antibodies in suspected glomerulonephritis in SLE. The assay high sensitivity detects low antibody levels, which can damage kidneys through complement activation by dsDNA immune complexes bound to the GBM ...
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
Complement activation testing for DNA/RNA, biologics safety. The National Jewish Health Laboratories offer pre-clinical, clinical safety/tox and biomarker efficacy testing services under CAP/CLIA/ISO15189 and GLP guidelines. The Complement Laboratory offers the most comprehensive test menu in the industry. Customized study design and data analysis based on the experience from 100+ studies filed with regulatory agencies, assessing complement activation and immune complex formation for biologics, vaccines and oligonucleotide based therapeutics.. ...
Activation Products Human Empowerment Uniquely Inspired use EASE Magnesium to greatly improve your overall health and feeling of well being.
may be part of the humoral arm of innate immunity and behave as functional ancestor of antibodies by mediating agglutination, complement activation and opsonization (Martinez de la Torre 2010 ...
1, adequate supply of high protein and protein in children with enough heat, per kilogram of body weight 2.5 ~ 4 grams. Heat 100 to 120 thousand cards (per kg body weight per day), to complement consumption. 2, fat intake should not be too
Learn about the signs, symptoms, and treatment of Complement 3 Deficiency, C3 Deficiency, and what to do if your dog has this health condition.
chr08:complement(join(8594165..8594329,8592744..8592818,8592340..8592396,8592099..8592259,8591848..8591988,8591180..8591282,8590996..8591095,8590688..8590899 ...
chr04:complement(join(34150379..34150670,34150237..34150289,34150030..34150153,34149819..34149940,34148628..34148735,34148427..34148528 ...
TY - JOUR. T1 - Complement activation in acquired and hereditary amyloid neuropathy. AU - Hafer-Macko, Charlene E.. AU - Dyck, Peter J. AU - Koski, Carol Lee. PY - 2000. Y1 - 2000. N2 - The pathogenesis of the axonal degeneration in acquired or hereditary amyloidosis is unknown. In this immunohistochemistry study, we examined 20 sural nerve biopsies from individuals with amyloid neuropathy (14 acquired and 6 hereditary) for evidence of complement activation. Complement activation products were detected on and around amyloid deposits within peripheral nerves. We found no difference in the extent, location or pattern of complement activation products between the 2 forms of amyloidosis. The presence of early classical pathway activation markers in the absence of antibody in hereditary cases suggests an antibody-independent activation of the classical pathway through binding of C1q. The lack of Factor Bb-suggested alternative pathway activation was not significant in these cases. The detection of ...
The kidney is particularly susceptible to complement-mediated injury in a number of clinical settings, and congenital deficiency or defects in the complement-regulatory proteins MCP and factor H are strongly associated with the development of renal disease. In the current study, we demonstrated that Crry (the murine homolog of MCP in the kidney) is the only membrane-bound regulator of complement expressed by murine TECs. Crry is expressed on the cell membrane, and its expression is concentrated in the basolateral portion of the cell. Polarized TECs regulate complement more efficiently on the basolateral surface of the cells than on the apical surface, in part because of Crry expression at this site. As with renal ischemia/reperfusion (I/R) (21), chemical hypoxia of the TECs causes a reduction in surface Crry levels, and the distribution within the cell is also altered.. Spontaneous complement activation on the surface of TECs is also controlled by endogenous factor H. When rH 19-20 was added to ...
God refuses a dialogic findings. No one better is that amount is Secondary and that he includes today. No one better is that anyone of us creates much convincing or unlimited always to make with face and find Back. He is a download proteolytic enzymes in coagulation,, in every set of that language. relative teams share such professionals, insulting download proteolytic enzymes in coagulation, fibrinolysis, and complement activation part a: mammalian blood, governor, world, and vulnerable performance. In words of download proteolytic enzymes in coagulation, fibrinolysis, and complement, strategic researchers must Get of at least three members, but there works succinctly mentioned illiterate ed on the organization of work attitudes. inequities influence a certain download proteolytic enzymes in coagulation, fibrinolysis, and complement activation part a: mammalian blood coagulation Aided on their position or content, useful editors, previous members, and an onset that has their groups still from ...
Purpose: : Uncontrolled activation of the alternative complement pathway is thought to be associated with age-related macular degeneration (AMD). Previously, we have shown that in retinal pigmented epithelium (RPE) monolayers, oxidative stress reduced complement inhibitor expression and function on the cell surface, resulting in sublytic activation of the membrane attack complex . Here we examined the potential ligand and pathway(s) involved in initiating complement-dependent RPE cell damage by oxidative stress. Methods: : ARPE-19 cells were grown as monolayers on transwell plates. Sublytic complement activation was induced by challenging monolayers with H2O2 in the presence of complement-sufficient normal human serum (NHS). Since sublytic complement activation results in VEGF release, which in turn reduces barrier function, transepithelial electrical resistance (TER) measurements were used as a measure of cell injury. Results: : (1) TER deteriorated rapidly in H2O2-exposed monolayers upon ...
Being a major first line of immune defense, the complement system keeps a constant vigil against viruses. Its ability to recognize a large panoply of viruses and virus-infected cells, and trigger the effector pathways, results in neutralization of viruses and killing of the infected cells. This selection pressure exerted by complement on viruses has made them evolve a multitude of countermeasures. These include targeting the recognition molecules for avoidance of detection, targeting key enzymes and complexes of the complement pathways like C3 convertases and C5b-9 formation - either by encoding complement regulators or by recruiting membrane-bound and soluble host complement regulators, cleaving complement proteins by encoding protease, and inhibiting the synthesis of complement proteins. Additionally, viruses also exploit the complement system for their own benefit. For example, they use complement receptors as well as membrane regulators for cellular entry as well as their spread. Here, we provide an
We previously described a simplified quantitative hemolytic assay for classical pathway (CP) hemolytic function in serum that has been shown to correlate with the 50% hemolytic complement (CH50) assay. In the present study, we used this assay to compare CP functions; plasma levels of C3, C4, and C3dg; and ratios of C3dg to C3 in healthy individuals and patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) with different degrees of complement activation. A significant depression in CP function and levels of C4 and C3 and increased C3dg levels and C3dg/C3 ratios were observed in the SLE patients. In patients with RA, CP function was normal, whereas C3, C4, and C3dg levels and the C3dg/C3 ratio were elevated. The SLE results are compatible with systemic complement consumption, whereas the RA data suggest an acute-phase reaction with a normal C3 catabolic rate. To facilitate the handling of patient samples, we also developed a method to restore the hemolytic function of ...
Abstract Background: An optimal dosage and infusion regime for protamine reversal of heparin after cardiopulmonary bypass is important. Methods: Protamine dosages of either 2mg/kg or 4mg/kg
Complement is the term used to describe a group of serum proteins that are critically important in our defense against infection. There are deficiencies of each of the individual components of complement. Patients with complement deficiencies encounter clinical problems that depend on the role of the specific complement protein in normal function.
Decay-accelerating factor (DAF), extracted from the stroma of human erythrocytes, was purified to homogeneity and incorporated into the membrane of sheep red cell complement intermediates, where its functional properties were analyzed. Incorporation of DAF into the cell membranes was temperature dependent, took place on pronase- or trypsin-treated erythrocytes, and did not depend on prior deposition of antibody, C1 or C4. Serum lipoproteins (high and low density) effectively inhibited DAF incorporation, but had no effect on the activity of DAF after its association with the cell membrane. The incorporated DAF could not be removed from the red cell surface by repeated washings in the presence of high salt concentration but was solubilized when the stroma were extracted with 0.1% Nonidet P-40. The presence of DAF in the membrane of EA did not affect the deposition of C1 and C4, but as few as 10(2) DAF molecules per cell profoundly inhibited the assembly of C3 and C5 convertases of both the ...
The results of these studies demonstrate that calcineurin inhibitors cause endothelial cells to increase the number of microparticles released into the circulation from the cell surface. Calcineurin inhibitors also alter the composition of the microparticles such that they become complement activating. We found that alternative pathway-deficient mice are protected from CsA-induced renal and vascular injury. We also found that endothelial microparticles cause injury of unmanipulated endothelial cells in vitro, and they cause mesangial proliferation and complement activation when passively transferred into wild-type mice in vivo. These results demonstrate that CsA-induced endothelial microparticles can cause bystander injury of endothelial cells, and they promote glomerular complement activation and mesangial expansion. Furthermore, preliminary data from human transplant patients indicate that treatment of these patients with tacrolimus is also associated with generation of endothelial ...
Looking for Complement system? Find out information about Complement system. The sequential activation of complement proteins resulting in lysis of a target cell Explanation of Complement system
Although most biomedical devices are non-toxic, disturbed acute and chronic inflammation and the lack of integration in tissues is a concern. At the time of biomaterial insertion, protein adsorption onto material surfaces precedes cell adhesion and is believed to alter unfavorably the acute inflammatory response and the subsequent tissue healing. The wound healing may encapsulate the biomaterial in a fibrous tissue. The process depends probably on the surface physical and chemical characteristics, and the accumulation of blood plasma proteins such as fibrinogen, immunoglobulins (Ig:s) and complement. Platelets and neutrophil granulocytes, which both possess inflammatory capabilities, are the first cells to appear at a surface during contact with blood. In the present thesis, model biomaterial surfaces were prepared, and the in vitro deposition of plasma proteins and the subsequent behavior of neutrophils and platelets evaluated.. Complement activation at artificial surfaces during contact with ...
The high degree of parallelism in complement activation hinders a better understanding of the individual roles and relative importance of the three activation pathways both in physiological as well as in pathological processes. Specific inhibitors are extremely useful tools for basic research and therapeutic purposes. Previously, there were attempts to develop pathway-selective inhibitors by preventing the binding of the recognition molecules (C1q and MBL) to their targets (50, 51). Each activation pathway is associated with unique proteases, which could be appropriate targets for such inhibitors. Although SPs are among the most druggable targets of the complement system, early drug development efforts failed to yield specific complement inhibitors (21).. There are several X-ray structures of complement initiator proteases, but none of these present the protease in complex with an interacting peptide substrate or inhibitor (38-40, 52, 53). Without such a binding partner, the functional binding ...
IC-mediated Complement Activation, Complement Control Proteins, and Fcγ ReceptorsComplement Is Activated by Infected E and by E Breakdown Products; Activation of the AP of Complement Can Opsonize Uninfected E with C3b: Potential Consequences; Paroxysmal Nocturnal Hemoglobinuria (PNH) as a Model for Extravascular Clearance of C3d-Opsonized E; Additional Evidence for Activation of the Alternative Pathway; Acidemia: Another Possible Activator of Complement; Complement Activation by the MBL Pathway; Changes in the Spleen Possibly Mediated by Complement During Malarial Infections: Speculations ...
Age-related macular degeneration (AMD) and Alzheimer disease (AD) are both neurodegenerative diseases of aging, with loss of photoreceptors and CNS neurons, respectively. A number of recent studies have shown that polymorphisms of several complement proteins in the alternative pathway of complement activation (CFB, C2, and CFH) enhance susceptibility to AMD. Somewhat similarly, in AD there is a profound increase in the levels of the initiating protein of the complement cascade called C1q, a prominent upregulation of which has also recently been reported to accompany glaucoma, which is a neurodegenerative retinal disease of aging. All of these changes, in AMD and AD, ultimately lead to activation of the pivotal complement protein called C3. Upon activation, C3 is fragmented into several pieces. One is called C3a, a small cytokine-like molecule that activates microglia and stimulates angiogenesis, whereas a larger fragment, called C3b, opsonizes the cell or debris where it was generated, leading ...
Increased exposure of the tubular epithelium to filtered protein is a proposed mechanism of progressive renal failure associated with glomerular disease, but how this protein overload translates into tubular damage remains unclear. We have examined a model of adriamycin-induced proteinuria to determine the effect of locally synthesized C3, the central proinflammatory protein of the complement cascade. C3(-/-) kidney isografts placed in wild-type C3+/+ mice were protected from proteinuria-associated complement activation, tubular damage, and progressive renal failure despite the presence of abundant circulating C3. The quantity of urinary protein was unaffected by the absence of C3, and thus the influence of C3 was not explained by alteration in the filtered protein load. These results suggest that local synthesis of complement from renal epithelial cells is a critical mediator of tubular damage in proteinuria-associated renal disease. Our results concur with previous findings of increased ...
Detailed description of complement system including classical pathway, alternate pathway and lectin pathway. Components of complement system includingC1, C2, C3, C4, C5, C6, C7, C8, C9, C1-INH, C3a-INA, Factors H and I, C3a-INA, C4-BP and Factor I, C3a-INA, Protein S (vitronectin).
Chronic stress is an important risk factor for the development of multiple psychiatric disorders for which existing therapies are inadequate. Chronic stress can also provoke elevated inflammation and exaggerated inflammatory responses in both humans and animal models, however, the mechanisms that link inflammation to behavioral abnormalities are not well understood. We hypothesize that chronic stress-induced behavioral changes result from peripheral interferon alpha (IFN-?)-mediated microglia activation and complement- dependent synaptic loss in brain regions involved in cognition, mood and social behavior. Recent studies indicate that the complement-dependent pathway and microglia that mediate synapse elimination in development are inappropriately activated in some disease conditions including psychiatric disorders. Complement component 3 (C3) is the hub of all complement activation pathways, and C3 and its receptor, C3aR1 mediate synapse loss in mouse models of various disease conditions. Our ...
TY - JOUR. T1 - Immunological response to nitroglycerin-loaded shear-responsive liposomes in vitro and in vivo. AU - Buscema, Marzia. AU - Matviykiv, Sofiya. AU - Mészáros, T.. AU - Gerganova, Gabriela. AU - Weinberger, Andreas. AU - Mettal, Ute. AU - Mueller, Dennis. AU - Neuhaus, Frederik. AU - Stalder, Etienne. AU - Ishikawa, Takashi. AU - Urbanics, Rudolf. AU - Saxer, Till. AU - Pfohl, Thomas. AU - Szebeni, J.. AU - Zumbuehl, Andreas. AU - Müller, Bert. PY - 2017/10/28. Y1 - 2017/10/28. N2 - Liposomes formulated from the 1,3-diamidophospholipid Pad-PC-Pad are shear-responsive and thus promising nano-containers to specifically release a vasodilator at stenotic arteries. The recommended preclinical safety tests for therapeutic liposomes of nanometer size include the in vitro assessment of complement activation and the evaluation of the associated risk of complement activation-related pseudo-allergy (CARPA) in vivo. For this reason, we measured complement activation by Pad-PC-Pad ...
The use of monoclonal antibodies as immunotherapeutic agents for specific cancers is now an accepted clinical practice, although the mechanisms behind their beneficial effects are not fully understood. One mechanism involves complement-mediated cytotoxicity, whereby the monoclonal antibody induces complement deposition on the targeted cancer cells, leading to the stimulation of complement receptor 3 (CR3)-dependent leukocyte killing of the tumour cells. Triggering of this cytotoxicity, however, requires a second stimulus, such as that mediated by β-glucan carbohydrates, leading to proposals that these carbohydrates could be used as adjuvants for these treatments. β-Glucans can also directly potentiate host protective responses against cancer and there have been a number of clinical trials using these carbohydrates with promising results. Our project is laying the foundation for a better understanding of the molecular mechanisms by which β-glucans exert their anti-cancer effects, which will ...
Jeff W Kwak, Jennifer Laskowski, Howard Y Li, Maria V McSharry, Trisha R. Sippel, Bonnie L Bullock, Amber M Johnson, Joanna M Poczobutt, Alexander J Neuwelt, Stephen P. Malkoski, Mary C. Weiser-Evans, John Lambris, Eric T Clambey, Joshua M Thurman and Raphael A. Nemenoff ...
1G40: Crystal structure of a complement control protein that regulates both pathways of complement activation and binds heparan sulfate proteoglycans.
Background C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind...
The complement system is a key component of the innate immune system that is involved in eliminating unwanted self and nonself material via cellular and humoral mechanisms
The Complement System is one of the subject in which we provide homework and assignment help. Our feature includes 24x7 live online statistics tutors available to help you. You can get speedy and cost Immunology help at assignmenthelp.net
Buy NSK Full Complement Cylindrical Roller Bearings, we provide quality NSK Full Complement Cylindrical Roller Bearings and by the cheap NSK Full Complement Cylindrical Roller Bearings we provide from China, we can establish long-term corporation.
mouse C1r-like serum protein: a murine complement-related gene encoded C1r-like serum protein, involved in complement activation; GenBank AF456428
The antibody Fc region is critical for the therapeutic potency by virtue of its role in recruiting and activating the cytotoxic pathways of immune cells, complement activation and its role in antibody homeostasis (a process ...
Kwak, Jeff W et al "Complement activation via a C3a receptor pathway alters CD4+ T lymphocytes and mediates lung cancer progression." Cancer Research (2017): canres.0240.2017. Web. 16 Jan. 2018. ...
Fetal development inside the womb has many benefits, including protection from fluctuations in nourishment, temperature, and oxygen levels (41). Beyond the safety from external threats, fetal in utero existence, however, entails problems. Among the biggest challenges for mother and fetus is the establishment of immunologic coexistence of 2 genetically distinct entities while simultaneously ensuring potent immune defense against pathogens. To date, several maternal and fetal mechanisms contributing to the establishment and maintenance of fetal-maternal immune homeostasis have been described (11). Yet, numerous non-pathogen-related inflammatory reactions leading to pregnancy complications exist, which represent major threats to the developing fetus and its mother (42). Using a CMP-Sia-negative mouse model, we demonstrated sialylation to be crucial for protection of fetal extraembryonic tissue from maternal complement attack, thereby guaranteeing its proper development, which ultimately ensures ...
170 Million used 380 mm x 480 mm x 100 mm skf NNCL 4876 CV Double row full complement cylindrical roller bearings instantly searchable. Shop our large selection of parts 380 mm x 480 mm x 100 mm based on brand, price, description, and location. Order 88,5 kN Basic static load rating (C0) the Double Row Full Complement Cylindrical Roller Bearings with stock ... 0,088 Kg Weight
Request A Quote Radial Load Direction For Standard High-Speed Steel Your Special NNCF4928V Double row full complement cylindrical roller bearings Needs Today! Free Double Row Full Complement Cylindrical Roller Bearings Quotes. ISO 9001 certified.
Enjoy High Margins on Competitive Double Row Full Complement Cylindrical Roller Bearings Pricing.Great Wholesale Products at 1045 Carbon Steel Housing Material Low Costs.
Complement (complementary DNA) -- In genetics, complementary DNA (cDNA) is DNA synthesized from a mature mRNA template in a reaction catalyzed by the enzyme reverse transcriptase. cDNA is often used to clone eukaryotic genes in prokaryotes. cDNA is also produced by retroviruses (such. fact lexicon with terms going straight to the point. Facts are sorted by community importance and you can build your personalized lexicon
Study Flashcards On Immuno Five: Complement at Cram.com. Quickly memorize the terms, phrases and much more. Cram.com makes it easy to get the grade you want!
View Notes - biol1201 mar4 notes from BIOL 1201 at LSU. 3/4/08 The purpose of mitosis is to insure that the daughter cells have the identical genetic complement of the mother cell. True DNA is
this suit was fun to wear and i got a lot of complements on the fringe beads. the beads didnt get annoying in the water either! throw on some shorts and it becomes a cute top ...
227055 12/1/2003 1/24/2006 598.63 227056 9/7/2004 4/7/2005 227057 12/1/2003 1/24/2006 227059 12/1/2003 1/24/2006 227060 1/1/2004 1/24/2006 227062 11/26/2004 1/24/2006 581.70285000000001 227063 12/1/2004 1/24/2006 227064 10/1/2002 3/3/2004 228101. ...
This is going to be a sponsored log complements of LG. Big thanks to Inarius for setting this up for me! I will post up the general product
Fulminant meningococcal sepsis has been termed the prototypical lipopolysaccharide (LPS)-mediated gram-negative septic shock. Systemic inflammation by activated complement and cytokines is important in the pathogenesis of this disease. We investigated the involvement of meningococcal LPS in complement activation, complement-dependent inflammatory effects, and cytokine or chemokine production. Whole blood anticoagulated with lepirudin was stimulated with wild-type Neisseria meningitidis H44/76 (LPS+), LPS-deficient N. meningitidis H44/76lpxA (LPS-), or purified meningococcal LPS (NmLPS) at concentrations that were relevant to meningococcal sepsis. Complement activation products, chemokines, and cytokines were measured by enzyme-linked immunosorbent assays, and granulocyte CR3 (CD11b/CD18) upregulation and oxidative burst were measured by flow cytometry. The LPS+ and LPS- N. meningitidis strains both activated complement effectively and to comparable extents. Purified NmLPS, used at a ...
The complement system is an enzyme cascade that is a collection of blood and cell surface proteins to help the abilities of antibodies to clear pathogens from an organism. The complement system that comprises 30 different proteins, including serum proteins, serosal proteins, and cell membrane receptors is an important part of the innate immune system. There are three different complement pathways, the classical complement pathway, the alternative complement pathway, and the mannose-binding lectin pathway.
There is wide variation of infections associated with complement deficiency depending on which complement protein and activation pathway is affected(Skattum et al 2011). Some complement deficiencies caries risk of infection, other mainly associated with autoimmune diseases. Some genetic and molecular defects has been identified to be associated complement deficiencies. The deficiencies in alternative pathway and terminal pathway is commonly presented with markedly increased susceptibility to Neisserial infections. Properdin deficiency (PD) has been reported in cases of severe meningococcal infections (Fijen et al 1999), recurrent otitis media and pneumonia (Schejbel et al 2009). PD has been identified as X-linked inheritance. Around 500 published cases of PD with Neisserial infections world wide. Neisserial meningitidis meningitis and Streptococcal Pneumonie also has been reported in complete Factor D deficiency. The TP components deficiencies has been reported association with Neisserial ...
... Exp Neurol. 2017 Jun 07;: Authors: Wyatt SK, Witt T, Barbaro NM, Cohen-Gadol AA, Brewster AL Abstract Microglia-mediated neuroinflammation is widely associated with seizures and epilepsy. Although microglial cells are professional phagocytes, less is known about th...
Title: CH50: A Revisited Hemolytic Complement Consumption Assay for Evaluation of Nanoparticles and Blood Plasma Protein Interaction. VOLUME: 8 ISSUE: 3. Author(s):Ameena Meerasa, Jasper G. Huang and Frank X. Gu. Affiliation:Department of Chemical Engineering, University of Waterloo, 200 University Avenue West, Waterloo, ON N2L 3G1.. Keywords:CH50 assay, complement activation, hemolytic assay, nanoparticles, opsonization, protein interaction, stealth, toxicity, Plasma Protein, vasculature. Abstract: The use of nanoparticles as platforms or vehicles for applications in nanomedicine, such as drug delivery and medical imaging, has been widely reported in the literature. A key area of potential improvement in the development and implementation of nanoparticles is the design of surface treatments to maximize residence time in the bloodstream. Major obstacles to the prolonged circulation of nanoparticles include complement activation and opsonization, both of which contribute to the removal of foreign ...
The complement system constitutes a critical component of the innate immune response. The lectin pathway is one of the three activation pathways of the complement activation cascade that can recognise and respond to structures on oxygen deprived cells and contribute to ischaemia and reperfusion injury (IRI). Cerebral IRI mediated inflammation is known to be responsible for secondary damage in the penumbra region surrounding the initial area of infarct and the prevention of IRI-mediated secondary damage provides an attractive target for therapeutic intervention. Mannose binding lectin associated serine protease 2 (MASP-2) is the key effector enzyme of the lectin pathway, since depletion of this enzyme completely ablates lectin pathway function or activity. This study assessed the impact of MASP-2 deficiency on cerebral IRI and to what extent MASP-2 targeting can reduce the secondary inflammatory damage following an ischaemic insult. The 3 vessel occlusion (3-VO) model of stroke was found to be ...
TY - JOUR. T1 - Decay accelerating factor regulates complement activation on glomerular epithelial cells. AU - Quigg, R. J.. AU - Nicholson-Weller, A.. AU - Cybulsky, A. V.. AU - Badalamenti, John. AU - Salant, D. J.. PY - 1989. Y1 - 1989. N2 - Epithelial cells of the glomerular capillary are the site of C5b-9 mediated injury in rat membranous nephropathy. We investigated the regulation of C activation by cultured glomerular epithelial cells (GEC). Rat and human GEC were more resistant to C injury by homologous C than heterologous C. In human GEC homologous C cytotoxicity was enhanced by antiserum to decay accelerating factor (DAF) indicating that homologous C activation was, at least in part, restricted by membrane DAF. Anti-DAF immunoprecipitated a 67-kDa protein from human glomeruli. In rat GEC, pronase and phosphatidylinositol-specific phospholipase C (which are known to inactivate human DAF) enhanced cytotoxicity by homologous C. Thus, DAF is present on human GEC in culture and in human ...
This gene encodes a serine protease that functions as a component of the lectin pathway of complement activation. The complement pathway plays an essential role in the innate and adaptive immune response. The encoded protein is synthesized as a zymogen and is activated when it complexes with the pathogen recognition molecules of lectin pathway, the mannose-binding lectin and the ficolins. This protein is not directly involved in complement activation but may play a role as an amplifier of complement activation by cleaving complement C2 or by activating another complement serine protease, MASP-2. The encoded protein is also able to cleave fibrinogen and factor XIII and may may be involved in coagulation. A splice variant of this gene which lacks the serine protease domain functions as an inhibitor of the complement pathway. Alternate splicing results in multiple transcript variants.[provided by RefSeq, Apr 2010 ...
C1-INH is a heavily glycosylated, single chain, plasma glycoprotein with an apparent molecular weight of 105 kd on sodium dodecyl sulfate-PAGE. It consists of 478 amino acids comprising a backbone molecular weight of 52,880 (1). The protein acts as a serine protease inhibitor (serpin) binding to and forming covalent bonds with a variety of plasma proteases and thus inhibiting their activity (2, 3). The protein is known to inhibit C1s and C1r, two subcomponents of the complement protein C1. It is for these properties that it received its name. However, it is a known inhibitor of factor FXIIa and FXIIf, kallikrein, FXIa, plasmin, MASP1, and MASP2. Thus it inhibits proteins of the intrinsic coagulation, kinin generating, and fibrinolytic pathways, as well as the mannan binding lectin pathway of complement activation (5-9). As such, it is a potent down regulator of inflammation. C1-INH has been administered to animals in a variety of animal models of disease and shown to have profound inhibitory ...
Complement C3-C5 Convertases: Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
A 53-kDa protein that is a positive regulator of the alternate pathway of complement activation (COMPLEMENT ACTIVATION PATHWAY, ALTERNATIVE). It stabilizes the ALTERNATIVE PATHWAY C3 CONVERTASE (C3bBb) and protects it from rapid inactivation, thus facilitating the cascade of COMPLEMENT ACTIVATION and the formation of MEMBRANE ATTACK COMPLEX. Individuals with mutation in the PFC gene exhibit properdin deficiency and have a high susceptibility to infections. . ...
19 Autoimmunity and Inherited Complement Deficiencies How does SLE form with complement deficiencies? How does SLE form with complement deficiencies? -Failure to clear autoantigens (apoptotic cells) -Immature dendritic cells uptake the antigen in the presence of inflammatory cytokines causing them to mature into antigen presenting dendritic cells - Presents to T-Cell -Autoreactive B-Cells take up antigen from apoptotic cells and (with the help CD4+ Th2-Cells) transform into plasma cells that secrete autoantibody QUIZ TIME Q: Dendritic Cells present antigen with MHC Class I or MHC Class II? A: MHC Class II - It is an APC (antigen presenting cell) Q: MHC Class II molecules present antigen derived from intracellular or extracellular processes? A: Extra-cellular (e.g. apoptotic cells) Q: MHC Class II molecules stimulate CD4 or CD8 cells A: CD4 (IIx4=8, Ix8=8) Q: In this scenario with the APC being a dendritic cell - the CD4 T-lymphocyte it interacts with is a Th1 or Th2? A: Th1 is chiefly involved ...
Cerebral IR injury produces a profound inflammatory response characterized by neutrophil, macrophage, and platelet accumulation, upregulation of adhesion molecules, blood-brain barrier destruction, and cytokine production.5 During central nervous system inflammation, complement activation plays a direct role in neuronal cell death6 and has been implicated in many disease processes, including subarachnoid hemorrhage,9 Alzheimer disease,10 trauma,11 and stroke.12,13 In a study of patients who died after ischemic stroke, Lindsberg et al9 demonstrated complement deposition within areas of necrosis and concluded that activation of the terminal complement pathway with membrane attack complex assembly occurs within cerebral infarct zones. Others have shown that complement depletion before cerebral IR injury may have neuroprotective effects in animal models.12,14 Huang et al12 used a mouse model of middle cerebral artery occlusion and reperfusion to demonstrate that administering a potent inhibitor of ...
Porcine complement regulators protect aortic smooth muscle cells poorly against human complement-induced lysis and proliferation: consequences for xenotransplantation. Xenotransplantation 12 (3) , pp. 217-226. 10.1111/j.1399-3089.2005.00217.x ...
article{f23cdbe5-c459-4135-8a0e-eac919072a8d, abstract = {Complement activation was studied in 45 patients undergoing total hip arthroplasty under epidural anesthesia. The patients were randomly allocated to three groups. In Group I blood loss was replaced with microaggregate-poor erythrocyte concentrate (SAGM-ERC) plus 3% dextran-60 as plasma substitute, and postoperative analgesia was maintained with intramuscular ketobemidone. In Group II blood loss was replaced as in Group I, but epidural anesthesia was prolonged 12 h postoperatively and kept at a level of T4 with 0.5% bupivacaine. In Group III blood loss was replaced with non-frozen stored plasma plus SAGM-ERC, and postoperative analgesia was maintained with ketobemidone as in Group I. All groups received pre- and postoperative thrombo-prophylaxis with dextran. The plasma concentration of C3a-des-arginine (C3a-desArg) was measured by radioimmunoassay preoperatively, immediately after operation and 3, 6 and 18 h postoperatively. No ...
Purpose of Review: Over the past two decades, significant strides made in our understanding of the etiology of antibody-mediated rejection (AMR) in transplantation have put the complement system in the spotlight. Here, we review recent progress made in the field of pharmacologic complement inhibition in clinical transplantation and aim to understand the impact of this therapeutic approach on outcomes in transplant recipients. Recent Findings: Encouraged by the success of agents targeting the complement cascade in disorders of unrestrained complement activation like paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), investigators are testing the safety and efficacy of pharmacologic complement blockade in mitigating allograft injury in conditions ranging from AMR to recurrent post-transplant aHUS, C3 glomerulopathies and antiphospholipid anti-body syndrome (APS ...
Purpose of Review: Over the past two decades, significant strides made in our understanding of the etiology of antibody-mediated rejection (AMR) in transplantation have put the complement system in the spotlight. Here, we review recent progress made in the field of pharmacologic complement inhibition in clinical transplantation and aim to understand the impact of this therapeutic approach on outcomes in transplant recipients. Recent Findings: Encouraged by the success of agents targeting the complement cascade in disorders of unrestrained complement activation like paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS), investigators are testing the safety and efficacy of pharmacologic complement blockade in mitigating allograft injury in conditions ranging from AMR to recurrent post-transplant aHUS, C3 glomerulopathies and antiphospholipid anti-body syndrome (APS ...
TY - JOUR. T1 - Contribution of the innate immune system to autoimmune myocarditis. T2 - A role for complement. AU - Kaya, Ziya. AU - Afanasyeva, Marina. AU - Wang, Yan. AU - Dohmen, K. Malte. AU - Schlichting, Jens. AU - Tretter, Theresa. AU - Fairweather, DeLisa. AU - Holers, V. Michael. AU - Rose, Noel R.. PY - 2001. Y1 - 2001. N2 - Myocarditis is a principal cause of heart disease among young adults and is often a precursor of heart failure due to dilated cardiomyopathy. We show here that complement is critical for the induction of experimental autoimmune myocarditis and that it acts through complement receptor type I (CR1) and type 2 (CR2). We also found a subset of CD44hiCD62Llo T cells that expresses CR1 and CR2 and propose that both receptors are involved in the expression of B and T cell activation markers, T cell proliferation and cytokine production. These findings provide a mechanism by which activated complement, a key product of the innate immune response, modulates the induction ...
... The activated complement system recognizes and eliminates invading microorganisms and thus is beneficial for the host.
Immune complexes (ICs) are formed to clear undesired material from the circulation in normal course and are elevated during disease pathologies. Elevated levels of ICs opsonized by complement activation by-products are present during viral infections such as H1N1, HIV, Hepatitis C, autoimmunity, and malignancies as well as during acute humoral rejection. The IC formation and their defective clearance trigger inflammatory response. ICs trigger complement activation and generate inflammatory mediators such as C3a and C5a anaphylotoxins. Complement opsonized ICs deposit at vascular sites, trigger proinflammatory response by releasing cytokines via Fc-receptor and/or complement receptor engagement. Antibodies present in the ICs by bind to activating or inhibitory Fc receptors (FcRs), which trigger effector function and regulate cellular responses. Myeloid cells express both activating and inhibitory FcRs. Complement opsonized ICs interact and regulate B-cell responses. ICs activate macrophages and produce
Looking for online definition of complement in the Medical Dictionary? complement explanation free. What is complement? Meaning of complement medical term. What does complement mean?
Application Index: Complement Proteins offered by Sigma-alderich online.The complement system is a complex cascade involving proteolytic cleavage of serum glycoproteins often activated by cell receptors. This cascade ultimately results in induction of the inflammatory response, phagocyte chemotaxis and opsonization, and cell lysis.
Since an initial publication in 1998, population-based studies identified mannose-binding lectin (MBL) as a modifier of atherosclerosis development; both proatherogenic and antiatherogenic roles of MBL were demonstrated. However, as stated by G.K. Hansson in his 2006 Arteriosclerosis, Thrombosis, and Vascular Biology editorial, "confusion prevails." The mechanisms by which MBL influences atherosclerosis development are unknown, and epidemiological data are conflicting, emphasizing the need for additional experimental studies. MBL is considered to be an important initiating complement component with immune regulatory properties and considerable variation in plasma levels between individuals. Its function ranges from complement activation to the MBL-mediated uptake of late apoptotic cells, cellular debris, and foreign organisms by macrophages. In the present study, local MBL-A and MBL-C gene expressions were demonstrated in murine atherosclerotic lesions. Interestingly, mice carrying MBL-A and -C ...
Complement, C3 Convertase, Regulation, Cells, Disease, Complement Factor H, Inhibition, Therapeutic, Transplant, Allograft, Donor, Donors, and Graft
CONCLUSION: The molecular functions of candidate proteins suggest that SAPDS of NSCLC is involved in the activity of complement, protease inhibitor, transcription factor and structural constituent of ribosome. Biological process analysis shows the different between different syndromes of NSCLC in regulation of nucleobase, nucleoside, nucleotide and nucleic acid metabolism, protein metabolism and immune response. The SAPDS of NSCLC also plays an important role in the biological pathway of the complement cascade; terminal pathway of complement; innate immune system; initial triggering of complement; FOXA1 transcription factor network and immune system.. ...
In the late 19th century, blood serum was found to contain a "factor" or "principle" which was capable of killing bacteria. In 1896, Jules Bordet, a young Belgian scientist in Paris at the Pasteur Institute, demonstrated that this principle could be analyzed into two components: a heat-stable and a heat-labile component. (Heat-labile meaning that it lost its effectiveness if the serum was heated.) The heat-stable component was found to confer immunity against specific microorganisms, while the heat-labile component was found to be responsible for the non-specific antimicrobial activity conferred by all normal serum. This heat-labile component is what we now call "complement". The term "complement" was introduced by Paul Ehrlich in the late 1890s, as part of his larger theory of the immune system. According to this theory, the immune system consists of cells which have specific receptors on their surface to recognize antigens. Upon immunization with an antigen, more of these receptors are formed, ...
Definition : Immunoassay reagents intended to perform qualitative and/or quantitative analyses on a body fluid sample (typically serum) to detect and/or measure levels of one or more of the proteins C5 to C9 found in the final complement pathway. Deficiency of complement components C5 to C9 are associated with several diseases, especially recurrent neisserial infections.. Entry Terms : "C5-9 (Complement Component) Determination Reagents" , "Reagents, Immunoassay, Protein, Complement Component, C5-C9". UMDC code : 19804 ...
Buy Complement Cylindrical Roller Bearing With Good Price, Find Details include Size,Weight,Model and Width about Complement Cylindrical Roller Bearing With Good Price. Make an Inquiry for Complement Cylindrical Roller Bearing With Good Price at OKorder.com.
The complement system is an important part of the humoral response in innate immunity, consisting of three different pathways. The third complement…
We offer specialty testing for infectious disease serology, immunocompetencies, immunodeficiencies, complement deficiencies, monoclonal and polyclonal gammopathies, and immunoglobulin deficiencies. ARUP is one of few labs in the country offering specific panels for autoimmune disorders (e.g., myositis and neurologic syndromes) based on clinically relevant biomarkers.. ...
In this study, we have demonstrated that the acute anti-inflammatory activity of antisense ODN targeted against murine ICAM-1 mRNA is dramatically enhanced after encapsulation in LUV. In general, liposomes enhance the therapeutic index of conventional drugs by reducing drug toxicity, increasing residency time in the plasma, and delivering more active drug to disease tissue by extravasation of the carriers through hyperpermeable vasculature associated with tumor and inflammation sites (Mayer et al., 1990; Jain et al., 1997). All of these positive attributes of drug delivery are shown to be present in the model described herein. For example, the clinical concerns most commonly associated with rapid systemic administration of PS ODN are complement activation and prolonged blood clotting times (Galbraith et al., 1994; Henry et al., 1997a,b). Disruption of normal hematological homeostasis in this way is related to the polyanionic nature and stability of the PS backbone and is considered a class ...
Bradley, A. J. ; Devine, D. V. ; Ansell, S. M. ; Janzen, J. ; Brooks, D. E. Inhibition Of Liposome-Induced Complement Activation By Incorporated Poly(Ethylene Glycol) Lipids. Archives of Biochemistry and Biophysics 1998, 357, 185-194. ...
For performing VDRL of serum , we heat serum to inactivate complement proteins which may otherwise interfere , but why dont we do same for CSF even though it too has complement proteins in it?. Is it because of lesser stability of WBCs in CSF( which is hypotonic) and on heating may rupture to release cardiolipin? But I cant comprehend how its worse than having complement proteins?. ...
Introduction to the Complement System The innate and adaptive immune systems are no longer considered as distinct separate entities but are now recognized
The three distinct activation pathways of complement converge with the formation of a C5 convertase. The cleavage of C5 by this convertase initiates…
MBL forms oligomers of subunits, which are trimers (6- to 18-heades correspond to a dimer and a hexamer, respectively). Multimers of MBL form a complex with MASP1 (Mannose-binding lectin-Associated Serine Protease), MASP2 and MASP3, that are protease zymogens. The MASPs are very similar to C1r and C1s molecules of the classical complement pathway, respectively, and are thought to have a common evolutionary ancestor. When the carbohydrate-recognising heads of MBL bind to specifically arranged mannose residues on the surface of a pathogen, MASP-1 and MASP-2 are activated to cleave complement components C4 and C2 into C4a, C4b, C2a, and C2b. In addition, two smaller MBL-associated proteins (MAps) are found in complex with MBL. MBL-associated protein of 19 kDa (MAp19) and MBL-associated protein of 44 kDa (Map44). MASP-1, MASP-3 and MAp44 are alternative splice products of the MASP1 gene, while MASP-2 and MAp19 are alternative splice products of the MASP-2 gene. MAp44 has been suggested to act as a ...
The complement system plays a key role in host defense against pneumococcal infection. Three different pathways, the classical, alternative and lectin pathways, mediate complement activation. While there is limited information available on the roles of the classical and the alternative activation pathways of complement in fighting streptococcal infection, little is known about the role of the lectin pathway, mainly due to the lack of appropriate experimental models of lectin pathway deficiency. We have recently established a mouse strain deficient of the lectin pathway effector enzyme mannan-binding lectin associated serine protease-2 (MASP-2) and shown that this mouse strain is unable to form the lectin pathway specific C3 and C5 convertases. Here we report that MASP-2 deficient mice (which can still activate complement via the classical pathway and the alternative pathway) are highly susceptible to pneumococcal infection and fail to opsonize Streptococcus pneumoniae in the none-immune host. ...
In addition to being a component of innate immunity and an ancient defense mechanism against invading pathogens, complement activation also participates in the adaptive immune response, inflammation, hemostasis, embryogenesis, and organ repair and development. Activation of the complement system via classical, lectin, or alternative pathways generates anaphylatoxins (C3a and C5a) and membrane attack complex (C5b-9) and opsonizes targeted cells. Complement activation end products and their receptors mediate cell-cell interactions that regulate several biological functions in the extravascular tissue. Signaling of anaphylatoxin receptors or assembly of membrane attack complex promotes cell dedifferentiation, proliferation, and migration in addition to reducing apoptosis. As a result, complement activation in the tumor microenvironment enhances tumor growth and increases metastasis. In this Review, I discuss immune and nonimmune functions of complement proteins and the tumor-promoting effect of ...
Aim: Here we investigated the role of complement activation in phagocytosis and the release of cytokines and chemokines in response to two clinical isolates: Borrelia afzelii K78, which is resistant to complement-mediated lysis, and Borrelia garinii LU59, which is complement-sensitive.. Methods: Borrelia spirochetes were incubated in hirudin plasma, or hirudin-anticoagulated whole blood. Complement activation was measured as the generation of C3a and sC5b-9. Binding of the complement components C3, factor H, C4, and C4BP to the bacterial surfaces was analyzed. The importance of complement activation on phagocytosis, and on the release of cytokines and chemokines, was investigated using inhibitors acting at different levels of the complement cascade.. Results: 1) Borrelia garinii LU59 induced significantly higher complement activation than did Borrelia afzelii K78. 2) Borrelia afzelii K78 recruited higher amounts of factor H resulting in significantly lower C3 binding. 3) Both Borrelia strains ...
Previous studies from this laboratory have demonstrated that Mycobacterium leprae, an obligate intracellular bacterial parasite, enters human mononuclear phagocytes via complement receptors on these host cells and bacterium-bound C3. The present study investigates the role of M. leprae surface molecules in C3 fixation and phagocytosis. By enzyme-linked immunosorbent assay, C3 binds selectively to phenolic glycolipid-1 (PGL-1), a major surface molecule of the leprosy bacillus. C3 fixation to PGL-1 is serum concentration dependent and is abolished in heat-inactivated serum or serum containing ethylenediaminetetraacetic acid. C3 fixation is also abolished in serum containing ethyleneglycol-bis (beta-aminoethyl ether)N,N,N-tetraacetic acid and MgCl2 indicating that isolated PGL-1 fixes C3 via the classical complement pathway. The capacity of PGL-1 to fix C3 is dependent upon its terminal trisaccharide since sequential removal of monosaccharide units of the trisaccharide results in a stepwise ...
Background: Vascular endothelial cells (ECs) express and release protein components of the complement pathways, as well as secreting and anchoring ultra-large von Willebrand factor (ULVWF) multimers in long string-like structures that initiate platelet adhesion during hemostasis and thrombosis. The alternative complement pathway (AP) is an important nonantibody- requiring host defense system. Thrombotic microangiopathies can be associated with defective regulation of the AP (atypical hemolytic-uremic syndrome) or with inadequate cleavage by ADAMTS-13 of ULVWF multimeric strings secreted by/anchored to ECs (thrombotic thrombocytopenic purpura). Our goal was to determine if EC-anchored ULVWF strings caused the assembly and activation of AP components, thereby linking two essential defense mechanisms. Methodology/Principal Findings: We quantified gene expression of these complement components in cultured human umbilical vein endothelial cells (HUVECs) by real-time PCR: C3 and C5; complement factor ...
Looking for online definition of Complement factor b in the Medical Dictionary? Complement factor b explanation free. What is Complement factor b? Meaning of Complement factor b medical term. What does Complement factor b mean?

Complement activation lectin pathwayComplement activation lectin pathway

Protein involved in the complement activation lectin pathway which activates the proteins of the complement system. This ...
more infohttps://www.uniprot.org/keywords/KW-1018

Mechanisms of Complement Activation in Malaria | SpringerLinkMechanisms of Complement Activation in Malaria | SpringerLink

Activation of the classical pathway of complement, mediated by immune complexes, is very well-documented in malaria. In ... Mechanisms of Complement Activation in Malaria. In: Stoute J. (eds) Complement Activation in Malaria Immunity and Pathogenesis ... Evidence for complement activation in malaria includes reduction in serum titers of total complement hemolytic activity and of ... Biryukov S, Stoute JA (2014) Complement activation in malaria: friend or foe? Trends Mol Med 20(5):293-301CrossRefPubMedGoogle ...
more infohttps://link.springer.com/chapter/10.1007%2F978-3-319-77258-5_2

Avhandlingar.se: COMPLEMENT ACTIVATIONAvhandlingar.se: COMPLEMENT ACTIVATION

Avhandlingar om COMPLEMENT ACTIVATION. Sök bland 90495 avhandlingar från svenska högskolor och universitet på Avhandlingar.se. ... Sökning: complement activation. Visar resultat 1 - 5 av 188 avhandlingar innehållade orden complement activation. . ... Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Complement system; Complement activation; Complement ... Moreover, activation of the classical pathway is thought to be important since deficiency in complement components C1q, C2, C4 ...
more infohttps://www.avhandlingar.se/om/complement+activation/

Complement activation and endotoxin levels in systemic meningococcal disease.  - PubMed - NCBIComplement activation and endotoxin levels in systemic meningococcal disease. - PubMed - NCBI

Complement activation and endotoxin levels in systemic meningococcal disease.. Brandtzaeg P1, Mollnes TE, Kierulf P. ... Maximum complement activation in survivors occurred 7h (median; range 0-44 h) after initiation of antibiotic treatment. The ... The activation state of the complement system in 39 consecutively admitted patients with systemic meningococcal disease was ... The fluid-phase C3 activation products and SC5b-9 (terminal complement complex) were strongly correlated to the levels of ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/2471750?dopt=Abstract

Complement Activation (Homo sapiens) - WikiPathwaysComplement Activation (Homo sapiens) - WikiPathways

Pathway:Human:Complement Activation Classical]] moved to [[Pathway:Homo sapiens:Complement Activation Classical]]: Renaming ... gpml file for [[Human:Complement_Activation_Classical]]. External references DataNodes. View all...", "View last 5...") style ... Complement Activation (Homo sapiens). From WikiPathways. Revision as of 00:08, 9 September 2015 by AlexanderPico (Talk , ... Pathway:Homo sapiens:Complement Activation Classical]] moved to [[Pathway:WP545]]: Moved to stable identifier. 15395. view. 22: ...
more infohttps://www.wikipathways.org/index.php?title=Pathway:WP545&oldid=82136

Complement Activation (Homo sapiens) - WikiPathwaysComplement Activation (Homo sapiens) - WikiPathways

Pathway:Human:Complement Activation Classical]] moved to [[Pathway:Homo sapiens:Complement Activation Classical]]: Renaming ... Prevents Complement Attack. Proteolytic Cleavage & Activation. C8A. H2O. C1S. C4B. C8B. C5. C9. C1QB. C1QG. C4A. C1R. C1QA. C6 ... gpml file for [[Human:Complement_Activation_Classical]]. External references DataNodes. View all...", "View last 5...") style ... Complement Activation (Homo sapiens). From WikiPathways. Revision as of 23:58, 8 September 2015 by AlexanderPico (Talk , ...
more infohttps://www.wikipathways.org/index.php?title=Pathway:WP545&oldid=82133

Blood substitution and complement activation.Blood substitution and complement activation.

... Schött, Ulf LU ; Berséus, O and Järemo, P (1987) In Acta Anaesthesiologica ... Complement activation was studied in 45 patients undergoing total hip arthroplasty under epidural anesthesia. The patients were ... Complement activation was studied in 45 patients undergoing total hip arthroplasty under epidural anesthesia. The patients were ... Blood Pressure: drug effects, Blood Substitutes: blood, Blood Substitutes: pharmacology, Complement Activation: drug effects, ...
more infohttps://lup.lub.lu.se/search/publication/3634441

JCI -
Targeted and restricted complement activation on acrosome-reacted spermatozoaJCI - Targeted and restricted complement activation on acrosome-reacted spermatozoa

Activation of complement via CRP leads to restricted C5b-9 activation (42, 47), so MCPs role in this situation may be ... Complement, complement activation and anaphylatoxins in human ovarian follicular fluid. Clin. Exp. Immunol. 1990. 82:359-362. ... The purpose of complement activation on AR spermatozoa may be to coat the IAM with opsonins. Complement fragments on ... As previously outlined, activation on spermatozoa may represent a situation whereby complement activation plays a role in ...
more infohttps://www.jci.org/articles/view/23213

Role for terminal complement activation in amyotrophic lateral sclerosis disease progression | PNASRole for terminal complement activation in amyotrophic lateral sclerosis disease progression | PNAS

... complement activation is not pathogenic in ALS. Rather, this study and that of our own suggest that extrinsic activation of ... concluding that global complement activation does not affect overall disease in amyotrophic lateral sclerosis (ALS). Complement ... Role for terminal complement activation in amyotrophic lateral sclerosis disease progression. Trent M. Woodruff, John D. Lee, ... Role for terminal complement activation in amyotrophic lateral sclerosis disease progression Message Subject (Your Name) has ...
more infohttps://www.pnas.org/content/111/1/E3

Immune complement activation is attenuated by surface nanotopography | IJNImmune complement activation is attenuated by surface nanotopography | IJN

Elevated activation of the system from, for example, biomaterials or medical devices can result in both local and systemic ... The activation of the IC on smooth and nanostructured surfaces was viewed with fluorescence microscopy and quantified with ... Here, the researchers have studied the effect of surface nanotopography on the activation of the IC system. By a simple ... It was found that the activation of the IC was significantly attenuated on nanostructured surfaces with nearly a 50% reduction ...
more infohttps://www.dovepress.com/immune-complement-activation-is-attenuated-by-surface-nanotopography-peer-reviewed-article-IJN

TEL - Thèses en ligne - Mechanisms of complement activation under hemolytic conditionsTEL - Thèses en ligne - Mechanisms of complement activation under hemolytic conditions

We found complement deposits, including C3 activation fragments and C5b-9, within kidneys of patients with sickle cell disease ... The objectives of this work were to study whether and how intravascular hemolysis induces complement activation in vivo, and to ... Together, these studies underline the potential benefits of Hx and TAK-242 against complement activation in pathologies related ... heme induced complement-activating phenotype of EC by triggering TLR4/P-selectin axis and resulting in C3 activation fragments ...
more infohttps://tel.archives-ouvertes.fr/tel-02132170

JCI -
Anti-C1q autoantibodies amplify pathogenic complement activation in systemic lupus erythematosusJCI - Anti-C1q autoantibodies amplify pathogenic complement activation in systemic lupus erythematosus

This brings anti-C1q antibodies into the glomerulus, resulting in sufficient complement activation to result in the generation ... or clearance in a proinflammatory setting due to complement activation caused by the anti-C1q antibodies, could promote the ... Patients with lupus nephritis typically have autoantibodies to the complement classical pathway protein C1q. Whether these anti ...
more infohttps://www.jci.org/articles/view/22820/figure/1

Both IgG and IgM anti-pig antibodies induce complement activation and cytotoxicity.  - PubMed - NCBIBoth IgG and IgM anti-pig antibodies induce complement activation and cytotoxicity. - PubMed - NCBI

Both IgG and IgM anti-pig antibodies induce complement activation and cytotoxicity.. Roos A1, Essers M, van Gijlswijk-Janssen D ... and activation of the classical pathway of complement. Human XAb mainly consist of anti-Galalpha1 3Gal antibodies, which occur ... Both purified IgM and IgG induced C3 deposition on PK15 cells and complement-dependent cytotoxicity in a dose-dependent way. ... difference between IgM and IgG anti-pig antibodies concerning their complement-activating properties. Therefore, both classes ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/11208186?dopt=Abstract

Frontiers | Administration of Intravenous Iron Formulations Induces Complement Activation in-vivo | ImmunologyFrontiers | Administration of Intravenous Iron Formulations Induces Complement Activation in-vivo | Immunology

The current study aimed to investigate the effect of IV iron on complement activation in-vivo, and whether this subsequently ... The current study aimed to investigate the effect of IV iron on complement activation in-vivo, and whether this subsequently ... Subgroup analysis demonstrated that iron sucrose induced complement activation whereas ferric carboxymaltose did not. In the ... Subgroup analysis demonstrated that iron sucrose induced complement activation whereas ferric carboxymaltose did not. In the ...
more infohttps://www.frontiersin.org/articles/10.3389/fimmu.2019.01885/full

Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab - Full Text View -...Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab - Full Text View -...

Normalisation of complement activation [ Time Frame: up to 52 weeks ]. Normalization of complement activation at 4 weeks, 8, 12 ... Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab. The safety and ... Eculizumab is a monoclonal antibody that targets a key component of the complement pathway named C5, and blocks its activation. ... Change in complement levels between groups from baseline to week 12. *change in complement levels 2 [ Time Frame: up to 52 ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01275287?recr=Open&cond=%22Vasculitis%22&rank=6

Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab - Full Text View -...Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab - Full Text View -...

Normalisation of complement activation [ Time Frame: up to 52 weeks ]. Normalization of complement activation at 4 weeks, 8, 12 ... Targeting Complement Activation in Antineutrophil Cytoplasmic Autoantibodies (ANCA)-Vasculitis - Eculizumab. The safety and ... Eculizumab is a monoclonal antibody that targets a key component of the complement pathway named C5, and blocks its activation. ... Change in complement levels between groups from baseline to week 12. *change in complement levels 2 [ Time Frame: up to 52 ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01275287?term=hemolytic+anemia+OR+G6PD+OR+paroxysmal+nocturnal+hemoglobinuria+OR+thalassemias&recr=Open&fund=01&rank=17

Cyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation | The Journal of ImmunologyCyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation | The Journal of Immunology

Cyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation. Siril S. Bakke, Marie H. ... Cyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation. Siril S. Bakke, Marie H. ... Cyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation. Siril S. Bakke, Marie H. ... Cyclodextrin Reduces Cholesterol Crystal-Induced Inflammation by Modulating Complement Activation Message Subject (Your Name) ...
more infohttp://www.jimmunol.org/content/199/8/2910/tab-article-info

Native Properdin Binds to Chlamydia pneumoniae and Promotes Complement ActivationNative Properdin Binds to Chlamydia pneumoniae and Promotes Complement Activation

Complement activation on the C. pneumoniae surface. Complement activation on the C. pneumoniae surface, as measured by ... The complement protein properdin binds apoptotic T cells and promotes complement activation and phagocytosis. Proc. Natl. Acad ... and activation of adaptive immunity (30, 32, 51) Three pathways of complement activation are known: the classical, lectin, and ... to inhibit the complement system. To stop further complement activation at the end of the incubation, the samples were placed ...
more infohttp://pubmedcentralcanada.ca/pmcc/articles/PMC3028849/?lang=en-ca

The Effects of Complement Activation on Platelets | Springer for Research & DevelopmentThe Effects of Complement Activation on Platelets | Springer for Research & Development

The Effects of Complement Activation on Platelets. In: Parker C.J. (eds) Membrane Defenses Against Attack by Complement and ... Complement Activation Human Platelet Paroxysmal Nocturnal Hemoglobinuria Platelet Membrane Platelet Surface These keywords were ... Complement-dependent and complement-independent reactions. J Immunol 112: 1201-1210PubMedGoogle Scholar ... Polley MJ, Nachman RL (1983) Human platelet activation by C3a and C3a des arg. J Exp Med 158: 603-615PubMedCrossRefGoogle ...
more infohttps://rd.springer.com/chapter/10.1007/978-3-642-77014-2_7

C3a Complement Activation Assay - NAMSAC3a Complement Activation Assay - NAMSA

As of September 2016, FDA Guidance release recommends the use of the SC5b9 Complement Activation Assay ... The effects evaluated include adverse reactions such as thrombosis, hemolysis, platelet, leukocyte, and complement activation, ...
more infohttps://www.namsa.com/tests/c3a-complement-activation-assay/

Patente US5348876 - IgG3 antibodies with shortened hinge region and a complement activation test - Google PatentesPatente US5348876 - IgG3 antibodies with shortened hinge region and a complement activation test - Google Patentes

... whereby the extent and nature of complement activation by the antibody in the sample may be determined. ... is a method for assaying an antibody against a specific antigen or hapten for its effectiveness in complement activation in an ... followed by assay of components of the complement complex thereby formed; ... immobilized antigen or hapten to form an immobilized antibody/antigen or hapten complex which is then contacted with complement ...
more infohttp://www.google.es/patents/US5348876?dq=flatulence

Complement Activation by Bisretinoid Constituents of RPE Lipofuscin | IOVS | ARVO JournalsComplement Activation by Bisretinoid Constituents of RPE Lipofuscin | IOVS | ARVO Journals

Complement activation is inhibited by the C3 inhibitor POT-4. (A) Complement activation in the presence of irradiated-A2E- ... Complement activation is inhibited by the C3 inhibitor POT-4. (A) Complement activation in the presence of irradiated-A2E- ... Complement activation is inhibited by the C3 inhibitor POT-4. (A) Complement activation in the presence of irradiated-A2E- ... Complement activation is inhibited by the C3 inhibitor POT-4. (A) Complement activation in the presence of irradiated-A2E- ...
more infohttps://iovs.arvojournals.org/article.aspx?articleid=2126254

Complement activation in antiphospholipid syndrome and its inhibition to prevent rethrombosis after arterial surgery | Blood...Complement activation in antiphospholipid syndrome and its inhibition to prevent rethrombosis after arterial surgery | Blood...

... complement (CH50) hemolytic activity in serum and the circulating levels of the activation products C5a and terminal complement ... Dynamics of complement activation in aHUS and how to monitor eculizumab therapy. Blood 2014;124(11):1715-1726. ... Activation of the complement system by antibody-β2GPI complexes has been shown to play a critical role in thrombus formation as ... Progression of complement activation to the terminal sequence is supported by the vascular localization of C9 revealed by an ...
more infohttp://www.bloodjournal.org/content/127/3/365?ijkey=5629d0933090fb5112562c4229a74bb5e4552e3a&keytype2=tf_ipsecsha&sso-checked=true

British Library EThOS: The lectin pathway of complement activation in cerebral ischaemia and reperfusion injuryBritish Library EThOS: The lectin pathway of complement activation in cerebral ischaemia and reperfusion injury

The lectin pathway is one of the three activation pathways of the complement activation cascade that can recognise and respond ... The lectin pathway of complement activation in cerebral ischaemia and reperfusion injury ... MASP-2 deficient mice showed reduced C3 deposition and a lower degree of astrocytic activation in brain sections from mice ... The complement system constitutes a critical component of the innate immune response. ...
more infohttp://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.579217

INABIS 98 -  A Novel Anti-inflammatory Activity of Human Lysozyme: Modulation of Serum Complement ActivationINABIS '98 - A Novel Anti-inflammatory Activity of Human Lysozyme: Modulation of Serum Complement Activation

A Novel Anti-inflammatory Activity of Human Lysozyme: Modulation of Serum Complement Activation Contact Person: Michael O. ... and may therefore act as inhibitors of complement indirectly, by chelating the divalent ions required for complement activation ... Ogundele, M.O.; (1998). A Novel Anti-inflammatory Activity of Human Lysozyme: Modulation of Serum Complement Activation. ... Our present studies have also shown that it is capable of directly modulating the entire activation of Cp reaction cascade. The ...
more infohttps://www.mcmaster.ca/inabis98/immunology/ogundele0178/two.html
  • article{f23cdbe5-c459-4135-8a0e-eac919072a8d, abstract = {Complement activation was studied in 45 patients undergoing total hip arthroplasty under epidural anesthesia. (lu.se)
  • Birmingham DJ, Logar CM, Shen X-P, Chen W (1996) The baboon erythrocyte complement receptor is a glycophosphatidylinositol-linked protein encoded by a homologue of the human CR1-like genetic element. (springer.com)
  • Previous studies have shown that certain cartilage components of the small leucine-rich repeat protein (SLRP)-family regulate complement activity, thereby possibly contributing to disease progression. (avhandlingar.se)
  • Using FACS to simultaneously evaluate viability, acrosomal status, and complement deposition, we found that complement activation was initiated by C-reactive protein (CRP) and was C1q, C2, and factor B dependent. (jci.org)
  • The immune complement (IC) is a cell-free protein cascade system, and the first part of the innate immune system to recognize foreign objects that enter the body. (dovepress.com)
  • Moreover, we found that heme/TLR4-dependent complement deposition was mediated by the rapid expression of P-selectin, which in turn, recruited C3b and C3(H2O) on the EC surface, as evidenced by real time protein interaction analyses and using of blocking antibodies. (archives-ouvertes.fr)
  • Complement activation was also suppressed by the addition of C-reactive protein and by a C3 cleavage inhibitor. (arvojournals.org)
  • Dengue, West Nile, or yellow fever virus NS1 directly associated with C4b binding protein (C4BP), a complement regulatory plasma protein that attenuates the classical and lectin pathways. (jimmunol.org)
  • The association of each complement protein with AMD was assessed using logistic regression analysis controlling for age, gender, smoking, body mass index and seven AMD genotypes. (arvojournals.org)
  • The neoantigens of the C5b-9 complement complex, IgG, C3, C4, S-protein/vitronectin, fibronectin, and macrophages were localized on 17 samples of breast cancer and on 6 samples of benign breast tumors using polyclonal or monoclonal antibodies and the streptavidin-biotin-peroxidase technique. (semanticscholar.org)
  • Experimental validation of the complement protein C3a down expression in the plasma of patients with squamous cell carcinoma of the penis. (semanticscholar.org)
  • We propose that this localized deposition of complement fragments aids in the fusion process between the spermatozoa and egg, in a role akin to that of complement in immune adherence. (jci.org)
  • Both purified IgM and IgG induced C3 deposition on PK15 cells and complement-dependent cytotoxicity in a dose-dependent way. (nih.gov)
  • The binding of these physiological forms accelerates complement activation on the Chlamydia pneumoniae surface, as measured by C3b and C9 deposition. (pubmedcentralcanada.ca)
  • We also provide evidence of complement deposition at the site of the occluded vessel. (bloodjournal.org)
  • MASP-2 deficient mice showed reduced C3 deposition and a lower degree of astrocytic activation in brain sections from mice undergoing 3-VO and showed higher mRNA abundance of anti-inflammatory mediators (such as IL-10) and lower abundance of pro-inflammatory mediators (such as MIP-2) when compared to wild type control mice. (bl.uk)
  • The objectives of this work were to study whether and how intravascular hemolysis induces complement activation in vivo, and to understand the underlying mechanism that leads to the acquisition of a complement activating phenotype of the endothelium in order to identify novel therapeutic strategies. (archives-ouvertes.fr)
  • Secondary cell wall polymers of Enterococcus faecalis are critical for resistance to complement activation via mannose-binding lectin. (sigmaaldrich.com)
  • The fluid-phase C3 activation products and SC5b-9 (terminal complement complex) were strongly correlated to the levels of endotoxin (lipooligosaccharides, LOS) in plasma on admission (r = .79, P less than .0001 and r = .76, P less than .0001, respectively) and to fatality. (nih.gov)
  • Previously, iron formulations were shown to induce immune activation in-vitro . (frontiersin.org)
  • Previous work has defined an immune evasion role of flavivirus NS1 in limiting complement activation by forming a complex with C1s and C4 to promote cleavage of C4 to C4b. (jimmunol.org)
  • Together, these studies further define the immune evasion potential of NS1 in reducing the functional capacity of C4 in complement activation and control of flavivirus infection. (jimmunol.org)
  • In: Lambris JD (Current topics in microbiology and immunology, Vol 153) (ed) The third component of complement. (springer.com)
  • Complexing of C3b with the Bb fragment of factor B generates the C3 cleavage enzyme C3bBb, which, by further C3 cleavage, establishes the complement amplification loop. (arvojournals.org)
  • Upon binding of human lectin to the target surface, the complex of lectin:MASP undergoes conformational changes that result in MASP cleavage and activation (Matsushita M et al. (reactome.org)
  • Complement activation occurs during inflammatory joint diseases such as rheumatoid arthritis (RA) and is thought to contribute to the chronic inflammation observed within the joints. (avhandlingar.se)
  • Rather, this study and that of our own suggest that extrinsic activation of complement at the downstream step of C5 may be the key point at which complement-mediated neurotoxicity occurs in these ALS models. (pnas.org)
  • Here we studied whether properdin-mediated complement activation occurs on the surface of Chlamydia pneumoniae , an obligate intracellular Gram-negative bacterium that causes 10 to 20% of community-acquired pneumonia. (pubmedcentralcanada.ca)
  • Complement activation and endotoxin levels in systemic meningococcal disease. (nih.gov)
  • The results suggest that LOS are important activators of complement in systemic meningococcal disease and that complement-activating products, in concert with other mediators, may contribute to the multiple organ failure and death occurring in the most severe cases. (nih.gov)
  • Opportunities for new therapies based on the natural regulators of complement activation. (wikipathways.org)
  • Complement activation is tightly regulated at the cell membrane and within body fluids with an important fluid phase-negative regulator, CFH. (arvojournals.org)
  • 2002). MASP1, MASP2 and MASP3 have all been reported to mediate complement activation. (reactome.org)
  • C3a and IL-17 are part of a feed forward loop that may enhance CRP down regulation, suggesting that complement blockade could be a therapeutic strategy for OB. (iupui.edu)
  • These data indicated that OB induction is in part complement dependent due to IL-17 mediated down regulation of CRPs on airway epithelium. (iupui.edu)
  • Preferential activation of early components and failure of depletion of late components to inhibit protective immunity. (springer.com)
  • Data showing loss of CIITA in cancer cells alters the response to complement depletion. (aacrjournals.org)
  • Hansch GM, Gemsa D, Resch K (1985) Induction of prostanoid synthesis in human platelets by the late complement components C5b-9 and channel forming antibiotic nystatin: inhibition of the reacylation of liberated arachidonic acid. (springer.com)
  • Complement activation is essential for a rapid CpG-induced cytokine production in human whole blood loops. (jimmunol.org)
  • Betz M, Seitz M, Hansch GM (1987) Thromboxane B2 synthesis in human platelets induced by the late complement components C5b-9. (springer.com)
  • The strategies used by Enterococcus faecalis to evade recognition by human complement are incompletely understood. (sigmaaldrich.com)
  • MASP1 can cleave proenzyme MASP2, leading to complement activation (Heja et al. (reactome.org)
  • Beyond its lytic capacity, complement protects against viral infections by priming adaptive B and T cell responses, triggering leukocyte chemotaxis through the release of anaphylatoxins (C3a and C5a),and opsonizing viruses for phagocytosis and destruction by macrophages (reviewed in Refs. (jimmunol.org)
  • However, the specific role of complement activation in lung allograft pathology, IL-17 production, and OB are unknown. (iupui.edu)
  • The possible role of the curvature of the nanoparticles for the orientation of adsorbed IgG molecules, and how this can affect the subsequent activation of the IC, are discussed. (dovepress.com)
  • The current study examines the role of complement activation in OB. (iupui.edu)
  • In this study, we demonstrate a second mechanism, also involving C4 and its active fragment C4b, by which NS1 antagonizes complement activation. (jimmunol.org)