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Serum sickness in humans is a reaction to proteins in antiserum derived from a non-human animal source, occurring 5–10 days after exposure. Symptoms often include a rash , joint pain , fever , and lymphadenopathy .
The mechanism by which immune complexes are pathogenic is complex and much of what we know is derived from experimental models of the Arthus reaction and serum sickness. These models support that Fc receptors play a dominant role in the response which can be augmented by the complement system via the anaphylatoxin C5a.
[3] An example of complement dependent type II hypersensitivity is an acute hemolytic transfusion reaction following transfusion of ABO incompatible blood. [4] Preformed antibody (predominantly IgM) against donor red cell antigens not found in an individual of a particular blood group (e.g. anti-A IgM in an individual with blood group B), bind to the donor red cell surface and lead to rapid ...
Activation of the complement pathway. Antibody-dependent cellular cytotoxicity. The pathophysiology of type II hypersensitivity reactions can be broadly classified into three types: [10] Cell depletion or destruction without inflammation; Inflammation mediated by complement or Fc receptor; Cellular dysfunction by antibodies
In immunology, the Arthus reaction (/ ˌ ɑːr ˈ tj uː s /) is a type of local type III hypersensitivity reaction.Type III hypersensitivity reactions are immune complex-mediated, and involve the deposition of antigen/antibody complexes mainly in the vascular walls, serosa (pleura, pericardium, synovium), and glomeruli.
Complement deficiency is an immunodeficiency of absent or suboptimal functioning of one of the complement system proteins. [4] Because of redundancies in the immune system, many complement disorders are never diagnosed. Some studies estimate that less than 10% are identified. [5]
True serum sickness, a type III hypersensitivity reaction, results in fever, lymphadenopathy, arthralgias, cutaneous eruptions, gastrointestinal disturbances, proteinuria, and significant decreases in serum complement levels; it was originally described after patients were infused with equine immunoglobulins.
Complement component 3, often simply called C3, is a protein of the immune system that is found primarily in the blood. It plays a central role in the complement system of vertebrate animals and contributes to innate immunity. In humans it is encoded on chromosome 19 by a gene called C3. [5] [6]