Complement C3
Complement C4
Complement C4a
Complement C3a
Complement C1q
Complement C5a
Complement Activation
Complement C4b
Complement C5
Complement C3b
Complement System Proteins
Complement C6
Complement C3c
Complement C3d
Complement C2
Complement C9
Receptors, Complement
Complement C1s
Complement Membrane Attack Complex
Complement C1r
Complement Inactivator Proteins
Complement C7
Complement C3-C5 Convertases
Complement Factor B
Complement Pathway, Alternative
Complement Pathway, Classical
Complement C8
Complement C1
Receptors, Complement 3b
Complement Factor H
Complement C5b
Complement C2a
Receptor, Anaphylatoxin C5a
Complement Activating Enzymes
Complement Inactivating Agents
Complement Hemolytic Activity Assay
Complement C1 Inactivator Proteins
Receptors, Complement 3d
Anaphylatoxins
Complement Fixation Tests
Complement Factor D
Complement Factor I
Complement C4b-Binding Protein
Complement C3b Inactivator Proteins
Antigens, CD55
Complement C3-C5 Convertases, Classical Pathway
Complement C2b
Antigens, CD59
Cobra Venoms
Antigen-Antibody Complex
Steroid 21-Hydroxylase
Complement C3-C5 Convertases, Alternative Pathway
Complement C1 Inhibitor Protein
Immunoglobulin G
Hemolysis
Complement C3 Convertase, Alternative Pathway
Complement C5 Convertase, Classical Pathway
Molecular Sequence Data
Complement C3 Convertase, Classical Pathway
Antigens, CD46
Opsonin Proteins
Blood Proteins
Lupus Erythematosus, Systemic
Complement C5 Convertase, Alternative Pathway
Phagocytosis
Amino Acid Sequence
Complement Pathway, Mannose-Binding Lectin
Properdin
Complement C5a, des-Arginine
Macrophage-1 Antigen
Protein Binding
Neutrophils
Base Sequence
Kidney Glomerulus
Serum
Glomerulonephritis, Membranoproliferative
Immunoglobulin M
Schistosoma
Genetic Complementation Test
Enzyme-Linked Immunosorbent Assay
Mice, Knockout
Glomerulonephritis
Arteriolosclerosis
Major Histocompatibility Complex
Erythrocytes
Autoantibodies
Cells, Cultured
RNA, Messenger
Macrophages
Immunity, Innate
Peptide Fragments
Mutation
Rabbits
Disease Models, Animal
Cloning, Molecular
Binding Sites
Blood Bactericidal Activity
Antigens, CD
Electrophoresis, Polyacrylamide Gel
Mannose-Binding Lectin
Alleles
Antibodies
Complement C3 Nephritic Factor
Glycoproteins
Immunoglobulins
Haptoglobins
DNA
Surface Plasmon Resonance
Peptides, Cyclic
Lupus Nephritis
Antibodies, Antinuclear
Sequence Homology, Amino Acid
Blotting, Western
Cosmids
Polymerase Chain Reaction
Gene Expression Regulation
Biological Markers
Inflammation
Carrier Proteins
Mannose-Binding Protein-Associated Serine Proteases
Adrenal Hyperplasia, Congenital
Species Specificity
Kidney
Phenotype
Immunologic Factors
Protein Structure, Tertiary
Immunohistochemistry
Gene Dosage
Haplotypes
Membrane Proteins
HLA Antigens
Sequence Homology, Nucleic Acid
Gene Expression
Monocytes
Fibrinogen
Exons
B-Lymphocytes
Flow Cytometry
Antibody Formation
Serine Endopeptidases
Streptococcus pneumoniae
Collectins
Restriction Mapping
Genes
DNA Primers
C-Reactive Protein
Genotype
Up-Regulation
Lipopolysaccharides
Steroid Hydroxylases
Blotting, Northern
T-Lymphocytes
DNA, Complementary
Blotting, Southern
Cytokines
Macular Degeneration
Disease Susceptibility
Models, Molecular
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Reverse Transcriptase Polymerase Chain Reaction
Cell Membrane
Pedigree
Case-Control Studies
Polymorphism, Restriction Fragment Length
Gene Frequency
Guinea Pigs
Immune Adherence Reaction
Escherichia coli
Immunoelectrophoresis
Staphylococcus aureus
Transfection
Liver
Lung
Arthritis, Rheumatoid
Fluorescent Antibody Technique
Interleukin-6
Protein Conformation
Epithelial Cells
Structure-Activity Relationship
Gene Library
Signal Transduction
Genetic Predisposition to Disease
Hemoglobinuria, Paroxysmal
Polymorphism, Single Nucleotide
Immune Complex Diseases
C5a receptor and interleukin-6 are expressed in tissue macrophages and stimulated keratinocytes but not in pulmonary and intestinal epithelial cells. (1/771)
The anaphylatoxin derived from the fifth component of the human complement system (C5a) mediates its effects by binding to a single high-affinity receptor (C5aR/CD88), the expression of which has been traditionally thought to be restricted to granulocytes, monocytes, macrophages (Mphi), and cell lines of myeloid origin. Recent immunohistochemical data suggested that human bronchial and alveolar cells express C5aR as well. To reexamine the tissue distribution of human C5aR expression, transcription of the C5aR gene was investigated in normal and pathologically affected human lung (bronchopneumonia, tuberculosis), large intestine (acute appendicitis, Crohn's disease), and skin (pyogenic granuloma, lichen planus) using in situ hybridization. In contrast to previous evidence, C5aR mRNA could not be detected in pulmonary or intestinal epithelial cells, whereas keratinocytes in inflamed but not in normal skin revealed detectable levels of C5aR transcripts. Additionally, it could be documented that only migrating Mphi express C5aR mRNA, whereas sessile Mphi in normal tissues and epithelioid/multinucleated Mphi found in granulomatous lesions do not. Because C5a has been demonstrated to upregulate the expression of interleukin (IL)-6 in human monocytes, we also studied IL-6 gene transcription in parallel to the C5aR. IL-6 mRNA was detectable in many tissue Mphi. Surprisingly, a tight co-expression of C5aR and IL-6 mRNA was observed in keratinocytes from lesions of pyogenic granuloma and lichen planus. These results point to an as yet unknown role for C5a in the pathogenesis of skin disorders beyond its well-defined function as a chemoattractant and activator of leukocytes. (+info)Chimeric receptors of the human C3a receptor and C5a receptor (CD88). (2/771)
Chimeras were generated between the human anaphylatoxin C3a and C5a receptors (C3aR and C5aR, respectively) to define the structural requirements for ligand binding and discrimination. Chimeric receptors were generated by systematically exchanging between the two receptors four receptor modules (the N terminus, transmembrane regions 1 to 4, the second extracellular loop, and transmembrane region 5 to the C terminus). The mutants were transiently expressed in HEK-293 cells (with or without Galpha-16) and analyzed for cell surface expression, binding of C3a and C5a, and functional responsiveness (calcium mobilization) toward C3a, C5a, and a C3a as well as a C5a analogue peptide. The data indicate that in both anaphylatoxin receptors the transmembrane regions and the second extracellular loop act as a functional unit that is disrupted by any reciprocal exchange. N-terminal substitution confirmed the two-binding site model for the human C5aR, in which the receptor N terminus is required for high affinity binding of the native ligand but not a C5a analogue peptide. In contrast, the human C3a receptor did not require the original N terminus for high affinity binding of and activation by C3a, a result that was confirmed by N-terminal deletion mutants. This indicates a completely different binding mode of the anaphylatoxins to their corresponding receptors. The C5a analogue peptide, but not C5a, was an agonist of the C3aR. Replacement of the C3aR N terminus by the C5aR sequence, however, lead to the generation of a true hybrid C3a/C5a receptor, which bound and functionally responded to both ligands, C3a and C5a. (+info)Regulatory effects of endogenous protease inhibitors in acute lung inflammatory injury. (3/771)
Inflammatory lung injury is probably regulated by the balance between proteases and protease inhibitors together with oxidants and antioxidants, and proinflammatory and anti-inflammatory cytokines. Rat tissue inhibitor of metalloprotease-2 (TIMP-2) and secreted leukoprotease inhibitor (SLPI) were cloned, expressed, and shown to be up-regulated at the levels of mRNA and protein during lung inflammation in rats induced by deposition of IgG immune complexes. Using immunoaffinity techniques, endogenous TIMP-2 in the inflamed lung was shown to exist as a complex with 72- and 92-kDa metalloproteinases (MMP-2 and MMP-9). In inflamed lung both TIMP-2 and SLPI appeared to exist as enzyme inhibitor complexes. Lung expression of both TIMP-2 and SLPI appeared to involve endothelial and epithelial cells as well as macrophages. To assess how these endogenous inhibitors might affect the lung inflammatory response, animals were treated with polyclonal rabbit Abs to rat TIMP-2 or SLPI. This intervention resulted in significant intensification of lung injury (as revealed by extravascular leak of albumin) and substantially increased neutrophil accumulation, as determined by cell content in bronchoalveolar lavage (BAL) fluids. These events were correlated with increased levels of C5a-related chemotactic activity in BAL fluids, while BAL levels of TNF-alpha and chemokines were not affected by treatment with anti-TIMP-2 or anti-SLPI. The data suggest that endogenous TIMP-2 and SLPI dynamically regulate the intensity of lung inflammatory injury, doing so at least in part by affecting the generation of the inflammatory mediator, C5a. (+info)Effects of a new C5a receptor antagonist on C5a- and endotoxin-induced neutropenia in the rat. (4/771)
A new C5a receptor antagonist, the cyclic peptide Phe-[Orn-Pro-D-cyclohexylalanine-Trp-Arg], (F-[OPdChaWR]), was tested for its ability to antagonize the neutropenic effects of both C5a and endotoxin in rats. Human recombinant C5a (2 microg kg(-1) i.v.) caused rapid neutropenia, characterized by an 83% decrease in circulating polymorphonuclear leukocytes (PMNs) at 5 min. Administration of F-[OPdChaWR] (0.3-3 mg kg(-1) i.v.), did not affect the levels of circulating PMNs but, when given 10 min prior to C5a, it inhibited the C5a-induced neutropenia by up to 70%. Administration of E. Coli lipopolysaccharide (LPS, 1 mg kg(-1) i.v.) also caused neutropenia with an 88% decrease in circulating PMNs after 30 min. When rats were pretreated with F-[OPdChaWR] (0.3 - 10 mg kg(-1) i.v.) 10 min prior to LPS, there was a dose-dependent antagonism of the neutropenia caused by LPS, with up to 69% reversal of neutropenia observed 30 min after LPS administration. These findings suggest that C5a receptor antagonists may have therapeutic potential in the many diseases known to involve either endotoxin or C5a. (+info)Dynamics of a chemoattractant receptor in living neutrophils during chemotaxis. (5/771)
Persistent directional movement of neutrophils in shallow chemotactic gradients raises the possibility that cells can increase their sensitivity to the chemotactic signal at the front, relative to the back. Redistribution of chemoattractant receptors to the anterior pole of a polarized neutrophil could impose asymmetric sensitivity by increasing the relative strength of detected signals at the cell's leading edge. Previous experiments have produced contradictory observations with respect to receptor location in moving neutrophils. To visualize a chemoattractant receptor directly during chemotaxis, we expressed a green fluorescent protein (GFP)-tagged receptor for a complement component, C5a, in a leukemia cell line, PLB-985. Differentiated PLB-985 cells, like neutrophils, adhere, spread, and polarize in response to a uniform concentration of chemoattractant, and orient and crawl toward a micropipette containing chemoattractant. Recorded in living cells, fluorescence of the tagged receptor, C5aR-GFP, shows no apparent increase anywhere on the plasma membrane of polarized and moving cells, even at the leading edge. During chemotaxis, however, some cells do exhibit increased amounts of highly folded plasma membrane at the leading edge, as detected by a fluorescent probe for membrane lipids; this is accompanied by an apparent increase of C5aR-GFP fluorescence, which is directly proportional to the accumulation of plasma membrane. Thus neutrophils do not actively concentrate chemoattractant receptors at the leading edge during chemotaxis, although asymmetrical distribution of membrane may enrich receptor number, relative to adjacent cytoplasmic volume, at the anterior pole of some polarized cells. This enrichment could help to maintain persistent migration in a shallow gradient of chemoattractant. (+info)Human T cells express the C5a receptor and are chemoattracted to C5a. (6/771)
The anaphylatoxin C5a is a potent mediator of inflammation that exerts a broad range of activity on cells of the myeloid lineage. In this study, we present the first evidence that human T cells express the C5a receptor (C5aR) and are chemotactic to C5a. Using FACS analysis, we found that the C5aR was expressed at a low basal level on unstimulated T cells and was strikingly up-regulated upon PHA stimulation in a time- and dose-dependent manner. CD3+ sorted T cells as well as Jurkat T cells were shown to express C5aR mRNA as assessed by RT-PCR. Moreover, semiquantitative RT-PCR analysis demonstrated that C5aR mRNA was down-regulated in purified T cells upon long-term PHA stimulation. To demonstrate that C5a was biologically active on T cells, we investigated the chemotactic activity of C5a and observed that purified CD3+ T cells are chemotactic to C5a at nanomolar concentrations. Finally, using a combination of in situ hybridization and immunohistochemistry, we showed that the T cells infiltrating the central nervous system during experimental allergic encephalomyelitis express the C5aR mRNA. In summary, these results suggest that C5a exerts direct effects on T cells and could be involved in the trafficking of T cells under physiological and pathological conditions, including inflammatory diseases of the central nervous system. (+info)Hemodynamic changes induced by liposomes and liposome-encapsulated hemoglobin in pigs: a model for pseudoallergic cardiopulmonary reactions to liposomes. Role of complement and inhibition by soluble CR1 and anti-C5a antibody. (7/771)
BACKGROUND: Intravenous administration of some liposomal drugs can trigger immediate hypersensitivity reactions that include symptoms of cardiopulmonary distress. The mechanism underlying the cardiovascular changes has not been clarified. METHODS AND RESULTS: Anesthetized pigs (n=18) were injected intravenously with 5-mg boluses of large multilamellar liposomes, and the ensuing hemodynamic, hematologic, and laboratory changes were recorded. The significant (P<0.01) alterations included 79+/-9% (mean+/-SEM) rise in pulmonary arterial pressure, 30+/-7% decline in cardiac output, 11+/-2% increase in heart rate, 236+/-54% increase in pulmonary vascular resistance, 71+/-27% increase in systemic vascular resistance, and up to a 100-fold increase in plasma thromboxane B2. These changes peaked between 1 and 5 minutes after injection, subsided within 10 to 20 minutes, were lipid dose-dependent (ED50=4. 5+/-1.4 mg), and were quantitatively reproducible in the same animal several times over 7 hours. The liposome-induced rises of pulmonary arterial pressure showed close quantitative and temporal correlation with elevations of plasma thromboxane B2 and were inhibited by an anti-C5a monoclonal antibody (GS1), by sCR1, or by indomethacin. Liposomes caused C5a production in pig serum in vitro through classic pathway activation and bound IgG and IgM natural antibodies. Zymosan- and hemoglobin-containing liposomes and empty liposomes caused essentially identical pulmonary changes. CONCLUSIONS: The intense, nontachyphylactic, highly reproducible, complement-mediated pulmonary hypertensive effect of minute amounts of intravenous liposomes in pigs represents a unique, unexplored phenomenon in circulation physiology. The model provides highly sensitive detection and study of cardiopulmonary side effects of liposomal drugs and many other pharmaceutical products due to "complement activation-related pseudoallergy" (CARPA). (+info)Inhibition of a membrane complement regulatory protein by a monoclonal antibody induces acute lethal shock in rats primed with lipopolysaccharide. (8/771)
Rats pretreated with traces of LPS developed acute fatal shock syndrome after i.v. administration of a mAb that inhibits the function of a membrane complement regulatory molecule. Such a shock was not observed after the administration of large amounts of LPS instead of the mAb following LPS pretreatment. The lethal response did not occur in rats depleted of either leukocytes or complement, and a C5a receptor antagonist was found to inhibit the reaction. Furthermore, LPS-treated rats did not suffer fatal shock following the injection of cobra venom factor, which activates complement in the fluid phase so extensively as to exhaust complement capacity. Therefore, complement activation on cell membranes is a requirement for this type of acute reaction. (+info)There are two main types of hemolysis:
1. Intravascular hemolysis: This type occurs within the blood vessels and is caused by factors such as mechanical injury, oxidative stress, and certain infections.
2. Extravascular hemolysis: This type occurs outside the blood vessels and is caused by factors such as bone marrow disorders, splenic rupture, and certain medications.
Hemolytic anemia is a condition that occurs when there is excessive hemolysis of RBCs, leading to a decrease in the number of healthy red blood cells in the body. This can cause symptoms such as fatigue, weakness, pale skin, and shortness of breath.
Some common causes of hemolysis include:
1. Genetic disorders such as sickle cell anemia and thalassemia.
2. Autoimmune disorders such as autoimmune hemolytic anemia (AIHA).
3. Infections such as malaria, babesiosis, and toxoplasmosis.
4. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and blood thinners.
5. Bone marrow disorders such as aplastic anemia and myelofibrosis.
6. Splenic rupture or surgical removal of the spleen.
7. Mechanical injury to the blood vessels.
Diagnosis of hemolysis is based on a combination of physical examination, medical history, and laboratory tests such as complete blood count (CBC), blood smear examination, and direct Coombs test. Treatment depends on the underlying cause and may include supportive care, blood transfusions, and medications to suppress the immune system or prevent infection.
The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.
There are several subtypes of LES, including:
1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.
There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.
It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.
Idiopathic membranous nephropathy (IMN) is an autoimmune disorder that causes GNM without any identifiable cause. Secondary membranous nephropathy, on the other hand, is caused by systemic diseases such as lupus or cancer.
The symptoms of GNM can vary depending on the severity of the disease and may include blood in the urine, proteinuria, edema, high blood pressure, and decreased kidney function. The diagnosis of GNM is based on a combination of clinical findings, laboratory tests, and renal biopsy.
Treatment for GNM is aimed at slowing the progression of the disease and managing symptoms. Medications such as corticosteroids, immunosuppressive drugs, and blood pressure-lowering drugs may be used to treat GNM. In some cases, kidney transplantation may be necessary.
The prognosis for GNM varies depending on the severity of the disease and the underlying cause. In general, the prognosis for IMN is better than for secondary membranous nephropathy. With proper treatment, some patients with GNM can experience a slowing or stabilization of the disease, while others may progress to end-stage renal disease (ESRD).
The cause of GNM is not fully understood, but it is believed to be an autoimmune disorder that leads to inflammation and damage to the glomerular membrane. Genetic factors and environmental triggers may also play a role in the development of GNM.
There are several risk factors for developing GNM, including family history, age (GMN is more common in adults), and certain medical conditions such as hypertension and diabetes.
The main complications of GNM include:
1. ESRD: Progression to ESRD is a common outcome of untreated GNM.
2. High blood pressure: GNM can lead to high blood pressure, which can further damage the kidneys.
3. Infections: GNM increases the risk of infections due to impaired immune function.
4. Kidney failure: GNM can cause chronic kidney failure, leading to the need for dialysis or a kidney transplant.
5. Cardiovascular disease: GNM is associated with an increased risk of cardiovascular disease, including heart attack and stroke.
6. Malnutrition: GNM can lead to malnutrition due to decreased appetite, nausea, and vomiting.
7. Bone disease: GNM can cause bone disease, including osteoporosis and bone pain.
8. Anemia: GNM can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
9. Increased risk of infections: GNM increases the risk of infections due to impaired immune function.
10. Decreased quality of life: GNM can significantly decrease a person's quality of life, leading to decreased mobility, pain, and discomfort.
It is important for individuals with GNM to receive early diagnosis and appropriate treatment to prevent or delay the progression of these complications.
The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:
* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure
Glomerulonephritis can be caused by a variety of factors, including:
* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia
The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.
Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:
* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases
The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.
Arteriolosclerosis is often associated with conditions such as hypertension, diabetes, and atherosclerosis, which is the buildup of plaque in the arteries. It can also be caused by other factors such as smoking, high cholesterol levels, and inflammation.
The symptoms of arteriolosclerosis can vary depending on the location and severity of the condition, but may include:
* Decreased blood flow to organs or tissues
* Fatigue
* Weakness
* Shortness of breath
* Dizziness or lightheadedness
* Pain in the affected limbs or organs
Arteriolosclerosis is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, angiography, or blood tests. Treatment for the condition may include lifestyle changes such as exercise and dietary modifications, medications to control risk factors such as hypertension and high cholesterol, and in some cases, surgical intervention to open or bypass blocked arterioles.
In summary, arteriolosclerosis is a condition where the arterioles become narrowed or obstructed, leading to decreased blood flow to organs and tissues and potentially causing a range of health problems. It is often associated with other conditions such as hypertension and atherosclerosis, and can be diagnosed through a combination of physical examination, medical history, and diagnostic tests. Treatment may include lifestyle changes and medications to control risk factors, as well as surgical intervention in some cases.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:
* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.
Lupus Nephritis can cause a range of symptoms, including:
* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Fatigue
* Fever
* Joint pain
Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
There are three main forms of ACH:
1. Classic congenital adrenal hyperplasia (CAH): This is the most common form of ACH, accounting for about 90% of cases. It is caused by mutations in the CYP21 gene, which codes for an enzyme that converts cholesterol into cortisol and aldosterone.
2. Non-classic CAH (NCAH): This form of ACH is less common than classic CAH and is caused by mutations in other genes involved in cortisol and aldosterone production.
3. Mineralocorticoid excess (MOE) or glucocorticoid deficiency (GD): These are rare forms of ACH that are characterized by excessive production of mineralocorticoids (such as aldosterone) or a deficiency of glucocorticoids (such as cortisol).
The symptoms of ACH can vary depending on the specific form of the disorder and the age at which it is diagnosed. In classic CAH, symptoms typically appear in infancy and may include:
* Premature puberty (in girls) or delayed puberty (in boys)
* Abnormal growth patterns
* Distended abdomen
* Fatigue
* Weight gain or obesity
* Easy bruising or bleeding
In NCAH and MOE/GD, symptoms may be less severe or may not appear until later in childhood or adulthood. They may include:
* High blood pressure
* Low blood sugar (hypoglycemia)
* Weight gain or obesity
* Fatigue
* Mood changes
If left untreated, ACH can lead to serious complications, including:
* Adrenal gland insufficiency
* Heart problems
* Bone health problems
* Increased risk of infections
* Mental health issues (such as depression or anxiety)
Treatment for ACH typically involves hormone replacement therapy to restore the balance of hormones in the body. This may involve taking medications such as cortisol, aldosterone, or other hormones to replace those that are deficient or imbalanced. In some cases, surgery may be necessary to remove an adrenal tumor or to correct physical abnormalities.
With proper treatment, many individuals with ACH can lead healthy, active lives. However, it is important for individuals with ACH to work closely with their healthcare providers to manage their condition and prevent complications. This may involve regular check-ups, hormone level monitoring, and lifestyle changes such as a healthy diet and regular exercise.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
There are two main types of MD:
1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.
The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:
* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision
MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.
There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:
* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.
It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.
There are several types of disease susceptibility, including:
1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.
Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.
In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.
The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.
Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.
Examples of diseases with a known genetic predisposition:
1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.
Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."
The disorder is caused by mutations in the HBB gene that codes for the beta-globin subunit of hemoglobin. These mutations result in the production of abnormal hemoglobins that are unstable and prone to breakdown, leading to the release of free hemoglobin into the urine.
HP is classified into two types based on the severity of symptoms:
1. Type 1 HP: This is the most common form of the disorder and is characterized by mild to moderate anemia, occasional hemoglobinuria, and a normal life expectancy.
2. Type 2 HP: This is a more severe form of the disorder and is characterized by severe anemia, recurrent hemoglobinuria, and a shorter life expectancy.
There is no cure for HP, but treatment options are available to manage symptoms and prevent complications. These may include blood transfusions, folic acid supplements, and medications to reduce the frequency and severity of hemoglobinuria episodes.
The term "immune complex disease" was first used in the 1960s to describe a group of conditions that were thought to be caused by the formation of immune complexes. These diseases include:
1. Systemic lupus erythematosus (SLE): an autoimmune disorder that can affect multiple organ systems and is characterized by the presence of anti-nuclear antibodies.
2. Rheumatoid arthritis (RA): an autoimmune disease that causes inflammation in the joints and can lead to joint damage.
3. Type III hypersensitivity reaction: a condition in which immune complexes are deposited in tissues, leading to inflammation and tissue damage.
4. Pemphigus: a group of autoimmune diseases that affect the skin and mucous membranes, characterized by the presence of autoantibodies against desmosomal antigens.
5. Bullous pemphigoid: an autoimmune disease that affects the skin and is characterized by the formation of large blisters.
6. Myasthenia gravis: an autoimmune disorder that affects the nervous system, causing muscle weakness and fatigue.
7. Goodpasture's syndrome: a rare autoimmune disease that affects the kidneys and lungs, characterized by the presence of immune complexes in the glomeruli of the kidneys.
8. Hemolytic uremic syndrome (HUS): a condition in which red blood cells are destroyed and waste products accumulate in the kidneys, leading to kidney failure.
Immune complex diseases can be caused by various factors, including genetic predisposition, environmental triggers, and exposure to certain drugs or toxins. Treatment options for these diseases include medications that suppress the immune system, such as corticosteroids and immunosuppressive drugs, and plasmapheresis, which is a process that removes harmful antibodies from the blood. In some cases, organ transplantation may be necessary.
In conclusion, immune complex diseases are a group of disorders that occur when the body's immune system mistakenly attacks its own tissues and organs, leading to inflammation and damage. These diseases can affect various parts of the body, including the skin, kidneys, lungs, and nervous system. Treatment options vary depending on the specific disease and its severity, but may include medications that suppress the immune system and plasmapheresis.
C5a receptor
Anaphylatoxin
Complement component 4
Complement system
Acylation stimulating protein
Formyl peptide receptor 1
C3a receptor
C5AR2
Alternative complement pathway
Formyl peptide receptor 3
Formyl peptide receptor 2
Classical complement pathway
Leukocyte extravasation
Complement component 5
C3a (complement)
Inflammation
C5a peptidase
Cutaneous small-vessel vasculitis
Chemotaxis
Neuroinflammation
Eculizumab
Complement membrane attack complex
C5-convertase
L-Ribonucleic acid aptamer
Hypoalbuminemia
Acute hemolytic transfusion reaction
Avacopan
Complement component 5a
Diffuse proliferative nephritis
Zilucoplan
Pattern recognition receptor
Find-me signals
Neutrophil
Cryoglobulinemia
List of MeSH codes (D12.776.124)
Specialized pro-resolving mediators
History of Eglin Air Force Base
C3b
History of women in the United States
Outwood Academy Acklam
G protein-coupled receptor
C5a
Lockheed C-5 Galaxy
Complement C5a Human Enzyme | C5a Protein | ProSpec
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Recombinant Human Complement Component C5a (rHuC5a) - 江苏沃尔森生物科技有限公司
negative regulation of tumor necrosis factor production - Ontology Report - Rat Genome Database
negative regulation of dopamine secretion Antibodies | Invitrogen
...
Metabolomics - Funded Research
Chronic Urticaria: Practice Essentials, Background, Pathophysiology
Thieme E-Books & E-Journals - Revista Brasileira de Ginecologia e Obstetrícia / RBGO Gynecology and Obstetrics
Postoperative pain-from mechanisms to treatment : PAIN Reports
Biomarkers Search
Publication Detail
Fatal Nongroupable Neisseria meningitidis Disease in Vaccinated Patient Receiving Eculizumab - Volume 24, Number 8-August 2018 ...
Aristotelis Astreinidis
Receptor, Anaphylatoxin C5a | Profiles RNS
Publications - Neuroimmunology Laboratories | MD Anderson Cancer Center
Complement and the Regulation of T Cell Responses - PubMed
DailyMed - STANDARDIZED CAT HAIR injection, solution
Frontiers | The Ubiquitin-Proteasome System: Potential Therapeutic Targets for Alzheimer's Disease and Spinal Cord Injury
Cellular Components of the Immune System - Immunology; Allergic Disorders - Merck Manuals Professional Edition
C5
- Early...
MeSH Browser
Safeguarding the Foreigner Within | The Scientist Magazine®
Early activation of the host complement system is required to restrict central nervous system invasion and limit neuropathology...
Receptor19
- Acting via a classical G protein-coupled receptor, CD88, C5a and C5adesArg exert a number of effects essential to the innate immune response, while their actions at the more recently discovered non-G protein-coupled receptor, C5L2 (or GPR77), remain unclear. (nih.gov)
- C5L2: a controversial receptor of complement anaphylatoxin, C5a. (nih.gov)
- Notably, the pro-inflammatory complement factor C5a and its receptor have been found to be up-regulated in microglia in the immediate surroundings of cerebral amyloid plaques in different mouse models of AD. (nih.gov)
- 2. C5L2 is required for C5a-triggered receptor internalization and ERK signaling. (nih.gov)
- 3. Disruption of the complement anaphylatoxin receptor C5L2 exacerbates inflammation in allergic contact dermatitis. (nih.gov)
- 7. TLR activation enhances C5a-induced pro-inflammatory responses by negatively modulating the second C5a receptor, C5L2. (nih.gov)
- 8. The C5a receptor (C5aR) C5L2 is a modulator of C5aR-mediated signal transduction. (nih.gov)
- 15. Complement 5a receptor-mediated neutrophil dysfunction is associated with a poor outcome in sepsis. (nih.gov)
- 18. Allosterism in human complement component 5a ((h)C5a): a damper of C5a receptor (C5aR) signaling. (nih.gov)
- The Ribosomal Protein S19 Suppresses Antitumor Immune Responses via the Complement C5a Receptor 1. (uc.edu)
- Receptor, Anaphylatoxin C5a" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
- A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A. (umassmed.edu)
- This graph shows the total number of publications written about "Receptor, Anaphylatoxin C5a" by people in this website by year, and whether "Receptor, Anaphylatoxin C5a" was a major or minor topic of these publications. (umassmed.edu)
- Below are the most recent publications written about "Receptor, Anaphylatoxin C5a" by people in Profiles. (umassmed.edu)
- We are very pleased with the exceptional progress we have made in the past year with our lead drug candidate, vilobelimab, in several areas, as well as in advancing our pipeline with a new clinical asset, INF904, an orally available small molecule inhibitor of the C5a receptor. (yahoo.com)
- Vilobelimab is a first-in-class, chimeric monoclonal IgG4-kappa antibody that binds to C5a and inhibits its interaction with the C5a receptor. (empr.com)
- The active substance in Tavneos, avacopan, blocks the receptor (target) for a protein in the blood called complement 5a (or C5a), which forms part of the immune system (the body's natural defences). (europa.eu)
- When C5a attaches to its receptor, it activates immune cells called neutrophils, which contribute to the inflammation of small blood vessels in GPA and MPA. (europa.eu)
- By blocking the receptor for C5a, Tavneos is expected to reduce inflammation of blood vessels, thus improving the symptoms of the disease. (europa.eu)
Receptors13
- The widespread expression of C5a receptors throughout the body allows C5a to elicit a broad range of effects. (nih.gov)
- Small molecular probes for G-protein-coupled C5a receptors: conformationally constrained antagonists derived from the C terminus of the human plasma protein C5a. (nih.gov)
- 1. Receptors for complement C5a. (nih.gov)
- 4. Complement C5a receptors C5L2 and C5aR in renal fibrosis. (nih.gov)
- 6. The interaction between C5a and both C5aR and C5L2 receptors is required for production of G-CSF during acute inflammation. (nih.gov)
- 10. Functions of C5a receptors. (nih.gov)
- 19. Structure and characterization of a high affinity C5a monoclonal antibody that blocks binding to C5aR1 and C5aR2 receptors. (nih.gov)
- Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. (thieme-connect.com)
- they have receptors for the crystallizable fragment (Fc) region of immunoglobulin (Ig) G and for complement, which enable them to bind with immune complexes and present the complex to B cells in germinal centers of secondary lymphoid organs. (merckmanuals.com)
- B lymphocyte memory: role of stromal cell complement and FcγRIIB receptors. (microbiologyresearch.org)
- In previous work, we showed that during cognate T cell/APC interactions, immune cell-derived complement activates locally, yielding C3a and C5a that bind to C3a/C5a receptors (C3aR/C5aR) on both partners ( 5 ). (diabetesjournals.org)
- Toll-like receptors (TLRs) and complement are 2 components of innate immunity that are critical for first-line host defense and elicitation of adaptive immune responses. (nih.gov)
- The regulatory effect of complement on TLR-induced cytokine production in vivo was mediated by the anaphylatoxin receptors C5aR and C3aR. (nih.gov)
Peptide1
- An activation peptide, C5a, which is an anaphylatoxin, which has potent spasmogenic and chemotactic activity, is derivative from the alpha polypeptide via cleavage with a convertase. (prospecbio.com)
Anaphylatoxins1
- Another immunologic mechanism for mast cell degranulation is mediated by complement-derived anaphylatoxins C3a, C4a and C5a. (nih.gov)
Monoclonal antibody2
Inhibitor1
- The TLR ligands lipopolysacharride (TLR4), zymosan (TLR2/6), and CpG oligonucleotide (TLR9) caused, in a complement-dependent manner, strikingly elevated plasma interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and IL-1beta, and/or decreased plasma IL-12 levels in mice deficient in the membrane complement inhibitor decay-accelerating factor (DAF). (nih.gov)
Potent spasmogenic and chemotactic activity1
- Cleavage of the alpha chain by a convertase enzyme results in the formation of the C5a anaphylatoxin, which possesses potent spasmogenic and chemotactic activity, and the C5b macromolecular cleavage product, a subunit of the membrane attack complex (MAC). (nih.gov)
Neutrophils1
- 12. A pro-inflammatory role of C5L2 in C5a-primed neutrophils for ANCA-induced activation. (nih.gov)
Activates1
- 1 C5a activates innate immune system responses, including inflammation and the release of histamines, and can increase damage to local tissues. (nih.gov)
Ascertain the role2
- In order to ascertain the role that complement plays in resolving VEEV-induced disease, complement-deficient C3 −/− mice were infected with a VEEV mutant (V3533) that caused mild, transient disease in immunocompetent mice. (microbiologyresearch.org)
- In this study, our goal was to ascertain the role of complement C3 in autoimmune diabetes. (diabetesjournals.org)
Inflammation1
- From NCBI Gene: This gene encodes a component of the complement system, a part of the innate immune system that plays an important role in inflammation, host homeostasis, and host defense against pathogens. (nih.gov)
Spasmogenic1
- C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. (nih.gov)
Chemotaxis1
- C5a has an imperative role in chemotaxis and C5b forms the 1st part of the complement membrane attack complex. (prospecbio.com)
C5aR3
- Role of C5a-C5aR axis in the development of atherosclerosis. (nih.gov)
- 14. Functional roles for C5a and C5aR but not C5L2 in the pathogenesis of human and experimental cerebral malaria. (nih.gov)
- 17. C5a and C5aR are elevated in joints of rheumatoid and psoriatic arthritis patients, and C5aR blockade attenuates leukocyte migration to synovial fluid. (nih.gov)
Peptides1
- In this study the authors tested the efficacy of active immunization with C5a-peptides AFF1 and AFF2 in Tg2576 mice exhibiting either early or late stages of the AD-like disease. (nih.gov)
20231
- JENA, Germany, March 22, 2023 (GLOBE NEWSWIRE) -- InflaRx N.V. (Nasdaq: IFRX), a clinical-stage biopharmaceutical company developing anti-inflammatory therapeutics by targeting the complement system, today announced financial and operating results for the year ended December 31, 2022. (yahoo.com)
Fragment2
Component of complement2
- Complement C5 is the 5th component of complement, which plays a central role in inflammatory and cell killing processes. (prospecbio.com)
- Complement C5 is the fifth component of complement, which plays an important role in inflammatory and cell killing processes. (watson-bio.cn)
Antigen1
- In humans, the MHC is called the human leukocyte antigen (HLA) system and is located on the short arm of chromosome 6, near the complement genes. (medscape.com)
Protein4
- C5a protein is composed of alpha and beta polypeptide chains, which are linked by a disulfide bridge. (prospecbio.com)
- C5a protein solution contains 120 mM NaCl and 10mM HEPES, pH 7.2. (prospecbio.com)
- Complement C5, also named C3 and PZP-like alpha-2-macroglobulin domain-containing protein 4, is involved in the complement system and it is encoded by the C5 gene in human. (watson-bio.cn)
- The encoded preproprotein is proteolytically processed to generate multiple protein products, including the C5 alpha chain, C5 beta chain, C5a anaphylatoxin and C5b. (nih.gov)
Elicit1
- By inhibiting mitochondrial STAT3 to elicit Mito-ROS generation, C5a triggers the generation of NETs to promote the development of arterial thrombosis . (bvsalud.org)
Inflammatory response2
- Higher levels of C5a increase the inflammatory response, which may result in multiorgan failure following COVID-19 activation of the complement system. (empr.com)
- According to preclinical data, IFX-1 showed ability to control the inflammatory response-related tissue and organ damage via a selective blockade of C5a in the adaptive, randomised, controlled trial. (clinicaltrialsarena.com)
Membrane3
- The C5b macromolecular cleavage product forms a complex with the C6 complement component, and this complex is the basis for creation of the membrane attack complex, which includes supplementary complement components. (prospecbio.com)
- The C5b macromolecular cleavage product can form a complex with the C6 complement component, and this complex is the basis for formation of the membrane attack complex, which includes additional complement components. (watson-bio.cn)
- 3 Vilobelimab targets C5a, which is a product of complement activation, and preserves membrane attack complex function. (nih.gov)
Neutrophil2
- Complement C5a induces the generation of neutrophil extracellular traps by inhibiting mitochondrial STAT3 to promote the development of arterial thrombosis. (bvsalud.org)
- In vitro , NETosis was observed when C5a was added to neutrophil cultures , and this effect was reversed by PMX53. (bvsalud.org)
Therapeutic1
- Thus, C5a has been found to be a significant pathogenic driver in a number of immuno-inflammatory diseases, making C5a inhibition an attractive therapeutic strategy. (nih.gov)
Concentrations2
- We found that the plasma concentrations of C5a were higher in patients with ST-elevation myocardial infarction ( STEMI ) than in patients with angina and higher in mice with left common carotid artery (LCCA) thrombosis induced by FeCl3 than in control mice . (bvsalud.org)
- High concentrations of C5a have been reported in patients with severe COVID-19. (nih.gov)
Serum2
- Description: A sandwich quantitative ELISA assay kit for detection of Canine Complement Component 5a (C5a) in samples from serum or plasma. (lscwarsaw.com)
- Description: A sandwich quantitative ELISA assay kit for detection of Mouse Complement Component 5a (C5a) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (lscwarsaw.com)
Regulation3
- Inflammatory processes in AD are primarily triggered by the up-regulation of the complement system in response to misfolded and aggregated proteins or mislocalized nucleic acids and reactive microglia. (nih.gov)
- The complement system in regulation of adaptive immunity. (microbiologyresearch.org)
- We demonstrate here a widespread regulation of TLR signaling by complement in vivo. (nih.gov)
Innate immunity1
- The complement system is an evolutionarily ancient key component of innate immunity required for the detection and removal of invading pathogens. (nih.gov)
Adaptive immunity1
- More recently, complement has also emerged as a critical player in adaptive immunity via its ability to instruct both B and T cell responses. (nih.gov)
Gene3
- Complement Component C5a (C5a) is involved in the complement system and it is encoded by the C5 gene in human. (prospecbio.com)
- Mutations in this gene cause complement component 5 deficiency, a disease characterized by recurrent bacterial infections. (nih.gov)
- Coincident with the induced elevations in blood glucose levels, we documented alternative pathway complement component gene expression within the islets of the diabetic WT mice. (diabetesjournals.org)
Mice1
- A similar outcome was observed in wild-type mice cotreated with the TLR ligands and cobra venom factor, a potent complement activator. (nih.gov)
Molecular2
- Human Complement C5a produced in Human plasma having a molecular mass of 10.4 kDa. (prospecbio.com)
- Many pathogen-associated molecular patterns activate both TLR and complement, but whether and how these 2 systems, when coactivated in vivo, interact with each other has not been well studied. (nih.gov)
System3
- In particular, work on the impact of complement on T cell responses led to the surprising discoveries that the complement system also functions within cells and is involved in regulating basic cellular processes, predominantly those of metabolic nature. (nih.gov)
- In the absence of a functional complement system, peripheral inoculation with V3533 induced much more severe encephalitis. (microbiologyresearch.org)
- The complement system contributes to autoimmune injury, but its involvement in promoting the development of autoimmune diabetes is unknown. (diabetesjournals.org)
Alzheimer's1
- Complement-initiated neuroinflammation and its role in early stage Alzheimer's disease. (umassmed.edu)
Activation2
- The 74 amino acid glycoprotein, complement component 5a (C5a), is a potent pro-inflammatory mediator cleaved enzymatically from its precursor, C5, upon activation of the complement cascade. (nih.gov)
- Both the activating and inhibitory Fc γ Rs and the activation of different complement cascades contribute to the downstream effector functions in the antibody-mediated disease pathology. (hindawi.com)
Immune cells1
- Diapedesis-Induced Integrin Signaling via LFA-1 Facilitates Tissue Immunity by Inducing Intrinsic Complement C3 Expression in Immune Cells. (nih.gov)
Reactive1
- In addition, our data showed that C5a increased the production of mitochondrial reactive oxygen species (ROS) and that the promotion of NET formation by C5a was mitochondrial ROS (Mito-ROS) dependent. (bvsalud.org)
Role2
- The data reveal a key role for immune cell-derived C3 in the pathogenesis of murine multiple low-dose streptozotocin-induced diabetes and support the concept that immune cell mediated diabetes is in part complement-dependent. (diabetesjournals.org)
- InflaRx said in a statement: "Based on the company's existing pre-clinical research on the role of C5a in viral-induced pneumonia and the initial results from the BDB study, InflaRx has decided to initiate a clinical development programme with IFX-1 in Covid-19 patients with severely progressed pneumonia. (clinicaltrialsarena.com)
Factor1
- IFX-1 is a monoclonal anti-human complement factor C5a antibody designed to inhibit the biological activity of C5a. (clinicaltrialsarena.com)
Human1
- C5a Human is stable at 4°C if entire vial will be used within 2-4 weeks. (prospecbio.com)
Patients1
- These patients were given BDB-001, an anti-C5a antibody produced by the company's licensee Beijing Defengrei Biotechnology in China. (clinicaltrialsarena.com)
Found1
- Furthermore, we found that C5a induced the production of Mito-ROS by inhibiting mitochondrial STAT3 activity. (bvsalud.org)
Study1
- Hence, our study identifies complement C5a as a potential new target for the treatment and prevention of thrombosis . (bvsalud.org)