Type III hypersensitivity, also known as immune complex hypersensitivity, is an exaggerated immune response triggered by the formation of immune complexes. Immune complexes are formed when antibodies bind to antigens, leading to the formation of clumps or aggregates in the bloodstream. These complexes can then deposit in various tissues and organs, activating the immune response and causing damage.
In type III hypersensitivity reactions, large quantities of immune complexes are generated and subsequently deposited in tissues. This triggers an inflammatory response as immune cells, such as neutrophils, are recruited to the affected sites. Activation of these immune cells results in the release of inflammatory mediators, causing tissue damage and inflammation.
Clinical manifestations of type III hypersensitivity reactions can vary depending on the site of immune complex deposition. Common examples include systemic lupus erythematosus (SLE), rheumatoid arthritis, and certain forms of vasculitis. Symptoms may range from skin rashes, joint pain, and renal dysfunction to more severe manifestations like vasculitis, glomerulonephritis, and even organ failure.
Diagnosis of type III hypersensitivities usually involves a combination of clinical evaluation, laboratory tests, and imaging studies. Treatment often focuses on controlling inflammation using medications such as corticosteroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and immunosuppressive drugs. In some cases, removal of the underlying cause, such as an infection or exposure to certain drugs, may be necessary to halt the immune response and prevent further damage.
In summary, type III hypersensitivities are immunological reactions triggered by the deposition of immune complexes in tissues, leading to inflammation and tissue damage.
