Arthus Reaction: A dermal inflammatory reaction produced under conditions of antibody excess, when a second injection of antigen produces intravascular antigen-antibody complexes which bind complement, causing cell clumping, endothelial damage, and vascular necrosis.Vasculitis, Leukocytoclastic, Cutaneous: Disorder characterized by a vasculitic syndrome associated with exposure to an antigen such as a drug, infectious agent, or other foreign or endogenous substance. Its pathophysiology includes immune complex deposition and a wide range of skin lesions. Hypersensitivity or allergy is present in some but not all cases.Immune Complex Diseases: Group of diseases mediated by the deposition of large soluble complexes of antigen and antibody with resultant damage to tissue. Besides SERUM SICKNESS and the ARTHUS REACTION, evidence supports a pathogenic role for immune complexes in many other IMMUNE SYSTEM DISEASES including GLOMERULONEPHRITIS, systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC) and POLYARTERITIS NODOSA.Edema: Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.Receptor, Anaphylatoxin C5a: A G-protein-coupled receptor that signals an increase in intracellular calcium in response to the potent ANAPHYLATOXIN peptide COMPLEMENT C5A.Passive Cutaneous Anaphylaxis: An evanescent cutaneous reaction occurring when antibody is injected into a local area on the skin and antigen is subsequently injected intravenously along with a dye. The dye makes the rapidly occurring capillary dilatation and increased vascular permeability readily visible by leakage into the reaction site. PCA is a sensitive reaction for detecting very small quantities of antibodies and is also a method for studying the mechanisms of immediate hypersensitivity.Antigen-Antibody Complex: The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.Cobra Venoms: Venoms from snakes of the genus Naja (family Elapidae). They contain many specific proteins that have cytotoxic, hemolytic, neurotoxic, and other properties. Like other elapid venoms, they are rich in enzymes. They include cobramines and cobralysins.Complement C5a: The minor fragment formed when C5 convertase cleaves C5 into C5a and COMPLEMENT C5B. C5a is a 74-amino-acid glycopeptide with a carboxy-terminal ARGININE that is crucial for its spasmogenic activity. Of all the complement-derived anaphylatoxins, C5a is the most potent in mediating immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE), smooth MUSCLE CONTRACTION; HISTAMINE RELEASE; and migration of LEUKOCYTES to site of INFLAMMATION.Skin: The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.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).Receptors, Complement: Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.Receptors, IgG: Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).Neutrophil Infiltration: The diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions.Neutrophils: Granular leukocytes having a nucleus with three to five lobes connected by slender threads of chromatin, and cytoplasm containing fine inconspicuous granules and stainable by neutral dyes.Hypersensitivity, Delayed: An increased reactivity to specific antigens mediated not by antibodies but by cells.Hemorrhage: Bleeding or escape of blood from a vessel.Receptors, Fc: Molecules found on the surface of some, but not all, B-lymphocytes, T-lymphocytes, and macrophages, which recognize and combine with the Fc (crystallizable) portion of immunoglobulin molecules.Exudates and Transudates: Exudates are fluids, CELLS, or other cellular substances that are slowly discharged from BLOOD VESSELS usually from inflamed tissues. Transudates are fluids that pass through a membrane or squeeze through tissue or into the EXTRACELLULAR SPACE of TISSUES. Transudates are thin and watery and contain few cells or PROTEINS.Peritonitis: INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.Macrophages, Alveolar: Round, granular, mononuclear phagocytes found in the alveoli of the lungs. They ingest small inhaled particles resulting in degradation and presentation of the antigen to immunocompetent cells.Keratitis: Inflammation of the cornea.Peroxidase: A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC 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)Allergy and Immunology: A medical specialty concerned with the hypersensitivity of the individual to foreign substances and protection from the resultant infection or disorder.Immunoglobulin Heavy Chains: The largest of polypeptide chains comprising immunoglobulins. They contain 450 to 600 amino acid residues per chain, and have molecular weights of 51-72 kDa.Immunoglobulin Isotypes: The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties.Immunoglobulin Light Chains: Polypeptide chains, consisting of 211 to 217 amino acid residues and having a molecular weight of approximately 22 kDa. There are two major types of light chains, kappa and lambda. Two Ig light chains and two Ig heavy chains (IMMUNOGLOBULIN HEAVY CHAINS) make one immunoglobulin molecule.Greek World: A historical and cultural entity dispersed across a wide geographical area under the influence of Greek civilization, culture, and science. The Greek Empire extended from the Greek mainland and the Aegean islands from the 16th century B.C., to the Indus Valley in the 4th century under Alexander the Great, and to southern Italy and Sicily. Greek medicine began with Homeric and Aesculapian medicine and continued unbroken to Hippocrates (480-355 B.C.). The classic period of Greek medicine was 460-136 B.C. and the Graeco-Roman period, 156 B.C.-576 A.D. (From A. Castiglioni, A History of Medicine, 2d ed; from F. H. Garrison, An Introduction to the History of Medicine, 4th ed)Immunoglobulin gamma-Chains: Heavy chains of IMMUNOGLOBULIN G having a molecular weight of approximately 51 kDa. They contain about 450 amino acid residues arranged in four domains and an oligosaccharide component covalently bound to the Fc fragment constant region. The gamma heavy chain subclasses (for example, gamma 1, gamma 2a, and gamma 2b) of the IMMUNOGLOBULIN G isotype subclasses (IgG1, IgG2A, and IgG2B) resemble each other more closely than the heavy chains of the other IMMUNOGLOBULIN ISOTYPES.Consensus Development Conferences as Topic: Presentations of summary statements representing the majority agreement of physicians, scientists, and other professionals convening for the purpose of reaching a consensus--often with findings and recommendations--on a subject of interest. The Conference, consisting of participants representing the scientific and lay viewpoints, is a significant means of evaluating current medical thought and reflects the latest advances in research for the respective field being addressed.Disease Outbreaks: Sudden increase in the incidence of a disease. The concept includes EPIDEMICS and PANDEMICS.Delphi Technique: An iterative questionnaire designed to measure consensus among individual responses. In the classic Delphi approach, there is no interaction between responder and interviewer.Click Chemistry: Organic chemistry methodology that mimics the modular nature of various biosynthetic processes. It uses highly reliable and selective reactions designed to "click" i.e., rapidly join small modular units together in high yield, without offensive byproducts. In combination with COMBINATORIAL CHEMISTRY TECHNIQUES, it is used for the synthesis of new compounds and combinatorial libraries.Software: Sequential operating programs and data which instruct the functioning of a digital computer.Information Storage and Retrieval: Organized activities related to the storage, location, search, and retrieval of information.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.Microcomputers: Small computers using LSI (large-scale integration) microprocessor chips as the CPU (central processing unit) and semiconductor memories for compact, inexpensive storage of program instructions and data. They are smaller and less expensive than minicomputers and are usually built into a dedicated system where they are optimized for a particular application. "Microprocessor" may refer to just the CPU or the entire microcomputer.Autistic Disorder: A disorder beginning in childhood. It is marked by the presence of markedly abnormal or impaired development in social interaction and communication and a markedly restricted repertoire of activity and interest. Manifestations of the disorder vary greatly depending on the developmental level and chronological age of the individual. (DSM-V)ComputersDiphtheria-Tetanus-acellular Pertussis Vaccines: Combined vaccines consisting of DIPHTHERIA TOXOID; TETANUS TOXOID; and an acellular form of PERTUSSIS VACCINE. At least five different purified antigens of B. pertussis have been used in various combinations in these vaccines.Asperger Syndrome: A disorder beginning in childhood whose essential features are persistent impairment in reciprocal social communication and social interaction, and restricted, repetitive patterns of behavior, interests, or activities. These symptoms may limit or impair everyday functioning. (From DSM-5)Diphtheria-Tetanus-Pertussis Vaccine: A vaccine consisting of DIPHTHERIA TOXOID; TETANUS TOXOID; and whole-cell PERTUSSIS VACCINE. The vaccine protects against diphtheria, tetanus, and whooping cough.Editorial Policies: The guidelines and policy statements set forth by the editor(s) or editorial board of a publication.Complement Factor B: A glycine-rich, heat-labile serum glycoprotein that contains a component of the C3 CONVERTASE ALTERNATE PATHWAY (C3bBb). Bb, a serine protease, is generated when factor B is cleaved by COMPLEMENT FACTOR D into Ba and Bb.Glomerulonephritis: Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.Autoimmunity: Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.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 C2: A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.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.

Cutting edge: Fc receptor type I for IgG on macrophages and complement mediate the inflammatory response in immune complex peritonitis. (1/146)

The contributions of Fc receptors (FcRs) for IgG (FcgammaRs) and complement to immune complex (IC)-mediated peritonitis were evaluated in BALB/c-, C57BL/6-, FcRgamma chain-, and FcR type III for IgG (FcgammaRIII)-deficient mice, backcrossed to the C57BL/6 background. In BALB/c mice, but not in C57BL/6 mice, neutrophil migration was markedly attenuated after complement depletion. In mice lacking FcRgamma chain, neutrophil migration was abolished, whereas it was unaffected in FcgammaRIII-deficient mice. Huge amounts of TNF-alpha (TNF) were found in the peritoneal exudate of BALB/c and C57BL/6 mice but were absent in mice lacking FcRgamma chain or FcgammaRIII. Surprisingly, a functional inhibition of TNF in BALB/c and C57BL/6 mice had no effect on neutrophil infiltration. These data provide evidence that in IC peritonitis, the activation of FcR type I for IgG on peritoneal macrophages and the activation of the complement cascade, but not the interaction of ICs with FcgammaRIII and the subsequent release of TNF, initiate the inflammatory response in BALB/c and C57BL/6 mice.  (+info)

Selection of a C5a receptor antagonist from phage libraries attenuating the inflammatory response in immune complex disease and ischemia/reperfusion injury. (2/146)

A C5a-receptor antagonist was selected from human C5a phage display libraries in which the C terminus of des-Arg74-hC5a was mutated. The selected molecule is a competitive C5a receptor antagonist in vitro and in vivo. Signal transduction is interrupted at the level of G-protein activation. In addition, the antagonist does not cause any C5a receptor phosphorylation. Proinflammatory properties such as chemotaxis or lysosomal enzyme release of differentiated U937 cells, as well as C5a-induced changes in intracellular Ca2+ concentration of murine peritoneal macrophages, are inhibited. The in vivo efficacy was evaluated in three different animal models of immune complex diseases in mice, i.e., the reverse passive Arthus reaction in the peritoneum, skin, and lung. The i.v. application of the C5a receptor antagonist abrogated polymorphonuclear neutrophil accumulation in peritoneum and markedly attenuated polymorphonuclear neutrophil migration into the skin and the lung. In a model of intestinal ischemia/reperfusion injury, i.v. administration of the C5a receptor antagonist decreased local and remote tissue injury: bowel wall edema and hemorrhage as well as pulmonary microvascular dysfunction. These data give evidence that C5a is an important mediator triggering the inflammatory sequelae seen in immune complex diseases and ischemia/reperfusion injury. The selected C5a receptor antagonist may prove useful to attenuate the inflammatory response in these disorders.  (+info)

IL-1 and TNF receptor-deficient mice show decreased inflammation in an immune complex model of uveitis. (3/146)

PURPOSE: To determine the role of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) in the induction of uveitis by a reverse passive Arthus reaction (RPAR). METHODS: Human serum albumin (HSA) antiserum was injected into the vitreous of "knockout" or "double knockout" mice genetically deficient in IL-1 receptor type I (IL-1RI-/-), TNF receptors p55 and p75 (TNFR p55-/-/p75-/-), IL-1RI and TNFR p55 (IL-1RI-/-/TNFR p55-/-), and controls. Twenty-four hours later, animals were challenged with intravenous HSA. Eyes were enucleated 4 hours after antigen challenge, and inflammation was quantitated by counting cells on histologic sections. Interleukin-6 in aqueous humor was measured with a B9 cell bioassay. The distribution of immune complexes in eyes was observed by immunohistochemical staining for IgG and complement component C3. RESULTS: Four hours after antigen challenge, immune complexes were localized at the ciliary body and iris of receptor-deficient mice. A transient uveitis was most severe at this time. A significant reduction in the median number of infiltrating cells was found in TNFR p55-/-/p75-/- mice (4.8, n = 15), compared with controls (14.2, n = 20, P < 0.05). The median number of infiltrating cells was significantly reduced in IL-1RI-/- mice (knockout 2.6, n = 11; controls 7.4, n = 8, P < 0.005). Interleukin-1RI-/-/TNFR p55-/- mice had a strong reduction in infiltrating cells (knockout 1.6, n = 11; controls 27.3, n = 12, P = 0.002). Interleukin-6 activity in aqueous humor was reduced in IL-1RI-/-/TNFR p55-/- mice (P = 0.03) but not in TNFR p55-/-/p75-/- (P = 0.40) mice. Most IL-1RI-/-mice had no detectable aqueous humor IL-6, but this group was not statistically different from controls. CONCLUSIONS: In contrast to endotoxin-induced uveitis, both IL-1 and TNF appear to have critical roles in RPAR uveitis. When receptors for these cytokines were deleted, the severity of immune complex-induced uveitis was profoundly reduced.  (+info)

The Arthus reaction in rodents: species-specific requirement of complement. (4/146)

We induced reverse passive Arthus (RPA) reactions in the skin of rodents and found that the contribution of complement to immune complex-mediated inflammation is species specific. Complement was found to be necessary in rats and guinea pigs but not in C57BL/6J mice. In rats, within 4 h after initiation of an RPA reaction, serum alternative pathway hemolytic titers decreased significantly below basal levels, whereas classical pathway titers were unchanged. Thus the dermal reaction proceeds coincident with systemic activation of complement. The serine protease inhibitor BCX 1470, which blocks the esterolytic and hemolytic activities of the complement enzymes Cls and factor D in vitro, also blocked development of RPA-induced edema in the rat. These data support the proposal that complement-mediated processes are of major importance in the Arthus reaction in rats and guinea pigs, and suggest that BCX 1470 will be useful as an anti-inflammatory agent in diseases where complement activation is known to be detrimental.  (+info)

A codominant role of Fc gamma RI/III and C5aR in the reverse Arthus reaction. (5/146)

Recent attempts to specify the relative contribution of FcR and complement in various experimental systems of immune complex disease have led to opposing conclusions. As concluded in IgG FcRgamma-/- mice, manifestation of disease is almost exclusively determined by FcgammaR on effector cells, arguing for a minor role of complement. In contrast, data obtained with C5aR-/- mice suggested that, dependent on the tissue site, complement is more important than FcgammaR. In this paper, we demonstrate that, in response to IgG immune complex formation, FcgammaRI/III- and C5aR-mediated pathways are both necessary and only together are they sufficient to trigger the full expression of inflammation in skin and lung. Moreover, both effector systems are not entirely independent, suggesting an interaction between FcgammaR and C5aR. Therefore, FcgammaR-mediated responses can be integrated through C5aR activation, which may explain why these two receptor pathways have previously been considered to dominate each other.  (+info)

Contribution of B(2) receptors for bradykinin in arthus reaction-induced plasma extravasation in wild-type or B(2) transgenic knockout mice. (6/146)

The aim of the present study was to investigate the contribution of bradykinin (BK) B(1) and B(2) receptors in a model of type III hypersensitivity, the reverse passive Arthus reaction (RPA), in wild-type mice and transgenic B(2) knockout littermates. BK (10 microg mouse(-1)) or bovine serum albumin (0.5 mg mouse(-1)) induced a sustained Evans blue extravasation for more than 80 min in naive or rabbit anti-bovine serum albumin-treated mice (RPA model), respectively. The response to the two stimuli was prevented by the B(2) receptor antagonist, HOE-140, but not by [Leu(8)]desArg(9)-BK (B(1) receptor antagonist). In contrast to the wild-type littermates, RPA and bradykinin were unable to trigger an increase in plasma extravasation in B(2) knockout mice. Furthermore, endothelin-1 (5 microg mouse(-1)) and a selective NK-1 receptor agonist [Sar(9),Met (O(2))(11)]-SP (20 microg mouse(-1)), triggered a significant increase in peritoneal plasma extravasation in both wild-type and B(2) knockout animals. A pretreatment with indomethacin (200 microg mouse(-1)) significantly reduced the RPA-induced but not the BK-induced increase in Evans blue extravasation. Furthermore, RPA, but not BK, triggered a significant indomethacin-sensitive increase in peritoneal prostaglandin E(2) content. Our results suggest a pivotal role for B(2) receptors in the mechanism of plasma extravasation which occurs during the reverse passive Arthus reaction in the mouse. Moreover, our results suggest an important contribution of prostanoids in the plasma leakage mechanisms triggered by RPA but not by bradykinin.  (+info)

A new small molecule C5a receptor antagonist inhibits the reverse-passive Arthus reaction and endotoxic shock in rats. (7/146)

C5a is implicated as a pathogenic factor in a wide range of immunoinflammatory diseases, including sepsis and immune complex disease. Agents that antagonize the effects of C5a could be useful in these diseases. We have developed some novel C5a antagonists and have determined the acute anti-inflammatory properties of a new small molecule C5a receptor antagonist against C5a- and LPS-induced neutrophil adhesion and cytokine expression, as well as against some hallmarks of the reverse Arthus reaction in rats. We found that a single i.v. dose (1 mg/kg) of this antagonist inhibited both C5a- and LPS-induced neutropenia and elevated levels of circulating TNF-alpha, as well as polymorphonuclear leukocyte migration, increased TNF-alpha levels and vascular leakage at the site of immune complex deposition. These results indicate potent anti-inflammatory activities of a new C5a receptor antagonist and provide more evidence for a key early role for C5a in sepsis and the reverse Arthus reaction. The results support a role for antagonists of C5a receptors in the therapeutic intervention of immunoinflammatory disease states such as sepsis and immune complex disease.  (+info)

Lyn is essential for fcgamma receptor III-mediated systemic anaphylaxis but not for the Arthus reaction. (8/146)

The Src family kinase Lyn initiates intracellular signal transduction by associating with a variety of immune receptors such as antigen receptor on B cells and high-affinity Fc receptor (FcR) for immunoglobulin Ig(E) (FcepsilonRI) on mast cells. Involvement of Lyn in the IgE-mediated immediate-type hypersensitivity is well documented, but the physiological significance of Lyn in IgG-dependent, type III low-affinity FcR for IgG (FcgammaRIII)-mediated responses is largely unknown. In this study, we generated a double-mutant mouse strain deficient in both type II FcR for IgG (FcgammaRIIB) and Lyn to exclude any involvement of inhibitory signaling by FcgammaRIIB, which otherwise downregulates FcgammaRIII-mediated cellular responses. FcgammaRIIB-deficient but Lyn-sufficient mice served as controls. The Lyn deficiency attenuated IgG-mediated systemic anaphylaxis in vivo, and significantly reduced calcium mobilization and degranulation responses of bone marrow-derived mast cells (BMMCs) in vitro. However, we found that either interleukin 4 or tumor necrosis factor alpha release by BMMCs was comparable to that from Lyn-deficient and control mice, and the reverse-passive Arthus reaction was equally induced in both mutant mice, indicating that Lyn is not involved in the onset of the IgG-mediated, FcgammaRIII-dependent late phase responses of mast cells. These findings provide us with insight into distinct signaling mechanisms in mast cells underlying the development of diverse pathologies as well as a therapeutic potential for selective treatment of allergic disorders.  (+info)

  • Studies with C5aR-deficient mice demonstrate a strongly reduced Arthus reaction in skin, lung, and peritoneum ( 9 ). (
  • Extraction of MPO from skin of C5aR (−/−) (striped bars) mice and their wild-type littermates (black bars) was performed 8 h after initiation of the Arthus reaction. (
  • The classical animal model for the inflammatory response in these IC diseases is the Arthus reaction, which features the infiltration of polymorphonuclear cells (PMN), hemorrhage, and plasma exudation ( 5 ). (
  • It has been proposed that the initiation of the inflammatory cascade depends almost entirely on mast cell FcγR-triggered activation leading to secondary reactions such as local complement production ( 14 , 15 ). (
  • It has long been accepted that IC-mediated activation of complement via the classical pathway represents the initial trigger of the Arthus response. (
  • ACIP has recommended that persons who experienced an Arthus reaction after a dose of tetanus toxoid-containing vaccine should not receive Td more frequently than every 10 years, even for tetanus prophylaxis as part of wound management. (
  • Killed vaccine does, however, produce hemagglutinin antibody and simultaneously incites later hypersensitivity to wild virus infection, producing the unusual dermatopathologic reaction seen. (
  • Many factors have influenced the use of vaccines among adults, including lack of awareness of safe vaccines and vaccine- preventable health burdens, unfounded concerns about adverse reactions, and missed opportunities by health-care providers to vaccinate adults during office, clinic, or hospital visits. (
  • You should not receive a booster vaccine if you had a life threatening allergic reaction after the first shot. (
  • Previous Arthus-type hypersensitivity reaction: not recommended until ≥10yrs after prior dose of tetanus toxoid-containing vaccine. (
  • According to the CDC, diphtheria, tetanus, and acellular pertussis vaccines (DTaP) should not be administered to any person who has experienced a severe allergic reaction to a previous dose or to anyone with a severe allergy to any ingredient found within the vaccine. (
  • As well, anyone who has experienced an Arthus-type hypersensitivity reaction following a previous dose of a diphtheria or tetanus toxoid containing vaccine should not receive another tetanus-diphtheria (Td) vaccine more frequently than every 10 years. (
  • Persons who experienced an Arthus-type hypersensitivity reaction following a prior dose of a tetanus toxoid-containing vaccine should not receive BOOSTRIX unless at least 10 years have elapsed since the last dose of a tetanus toxoid-containing vaccine. (
  • These include previous severe reaction to the vaccine or component, substantial suppression of cellular immunity, and pregnancy as contraindications. (
  • Dr. reported that his 12 yr old son was given a booster dose of Measles virus vaccine, live on 8-JUN-90 he experienced Arthus reaction consisting of synovitis of lt hip, inability to walk and pain at injection site. (
  • Although the organisms are absent, mycobacterial DNA has been detected in approximately half of the biopsy specimens subjected to polymerase chain reaction (PCR). (
  • Polymerase chain reaction (PCR) amplification for mycobacteria varies. (
  • More than 25% of the 16-26-year-old women enrolled in these trials had serological or polymerase chain reaction (PCR) evidence of previous or current infection with HPV-6, -11, -16, or -18. (
  • and specific side effects, adverse reactions, precautions, and contraindi- cations associated with use of these immunobiologics. (
  • Redness, swelling and pain at the injection site are the most common adverse reactions to acellular pertussis-containing vaccines. (
  • To report SUSPECTED ADVERSE REACTIONS, contact GlaxoSmithKline at 1-888-825-5249 or VAERS at 1-800-822-7967 or (
  • The classical animal model for the inflammatory response in these IC diseases is the Arthus reaction, which features the infiltration of polymorphonuclear cells (PMN), hemorrhage, and plasma exudation ( 5 ). (
  • Histamine had been described somewhat earlier by Dale and Laidlaw (1910) to mediate the anaphylactic shock defined by Portier and Richet (1902) as an unusual reaction of dogs to the injection of toxins isolated from the sea anemone Physalia . (
  • The accumulated evidence obtained so far show that mast cells are an integral part of the immunological surveillance system that act together with other immune cells to mount specific reactions in response to an inflammatory insult. (
  • It is the most severe form of an allergic reaction, where mast cells suddenly release a large amount of histamine and later on leukotrienes. (
  • An example here is the reaction to penicillin where the drug can bind to red blood cells causing them to be recognised as different, B cell proliferation will take place and antibodies to the drug are produced. (
  • Wolf-Jurgensen, 1965, 1967), the description of CBH focused renewed attention on the occurrence of basophils in delayed-onset immunologic reactions, particularly in the guinea pig. (
  • Supporting this concept, mice lacking FcRγ (deficient in both FcγRI and FcγRIII), but not C3-, C4-, and C5-deficient mice, show an impaired Arthus reaction ( 16 ). (
  • Hideo Kanauchi, Fukumi Furukawa , Takao Tachibana, Yuji Horiguchi, Sadao Imamura: Epidermal Langerhans cells in lesions of MRL/l mice and the Arthus reaction induced in guinea-pig skin. (
  • The results of this study indicate that both endothelial selectins contribute predominantly to the Arthus reaction by regulating mast cell and neutrophil infiltration and that the full development of the Arthus reaction is mediated cooperatively by all selectins and ICAM-1. (
  • Skin biopsies, obtained from three patients, demonstrate a combination of an Arthus reaction and delayed hypersensitivity. (
  • dill1971: If the allergic reaction is on your skin, you can try hydrocortisone cream to relieve the redness and the itching. (
  • Skin prick tests are helpful to test for food allergens that can trigger severe reactions, e.g., peanuts, eggs, fish, and milk. (
  • Takao Tachibana, Sinkichi Taniguchi, Fukumi Furukawa , Sadao Imamura: The time-dependent changes of serotonin-degrading enzymes activities in the Arthus reaction induced in guinea pig skin. (
  • Patients with cns infections describes a patients risk for active bleeding, history of arthus-type hypersensitivity reaction hypertension international aids societyusa intracranial hemorrhage iv, intravenous pe phenytoin equivalent. (