IIIhypersensitiviteitsreactie

IIIhypersensitiviteitsreactie, commonly referred to as type III hypersensitivity, is an immune complex–mediated reaction. It occurs when soluble antigen–antibody complexes form in circulation and deposit in tissues such as vessel walls, glomeruli, or the synovium. These deposits activate the complement system, generating anaphylatoxins like C3a and C5a that recruit and activate neutrophils. The ensuing inflammatory response and release of lytic enzymes cause tissue injury and fibrinoid necrosis in involved sites. The reaction often develops hours to days after exposure to the inciting antigen.

Common clinical contexts include serum sickness after exposure to heterologous proteins, the localized Arthus reaction following intradermal antigen exposure, and systemic autoimmune diseases such as systemic lupus erythematosus and cryoglobulinemia. Post-streptococcal glomerulonephritis is another classic example of immune complex–mediated injury. Pathologically, one finds granular deposits of immunoglobulins and complement in affected tissues. In vessels this may present as leukocytoclastic vasculitis; in the kidneys, immune complex–mediated glomerulonephritis may cause proteinuria and hematuria.

Diagnosis relies on clinical history and signs of immune complex–mediated inflammation, along with laboratory indicators such as hypocomplementemia and, when available, biopsy demonstrating immune complex and C3 deposition. Treatment aims to remove the inciting antigen and suppress inflammation, typically with corticosteroids; plasmapheresis or other immunosuppressive therapies are considered in severe cases. Management of the underlying disease or exposure is essential for resolution.