immuunkomplekside

Immune complexes, or immuunkomplekside in Estonian usage, are formed when antibodies bind soluble antigens, creating antigen–antibody complexes that can range from small to large. Under normal conditions, these complexes are cleared by the reticuloendothelial system, particularly in the liver and spleen, and do not cause harm.

Two broad forms exist: soluble immune complexes circulate in plasma; immune complexes that become deposited in tissues can trigger inflammation because they activate complement and engage Fc receptors on immune cells.

Formation and properties: The size and solubility of the complex influence its fate; large complexes are often cleared efficiently, while medium- to small-sized complexes can persist and deposit in tissues such as kidneys, joints, and skin.

Pathophysiology: Activation of the classical complement pathway by immune complexes leads to production of anaphylatoxins (C3a, C5a) and chemoattractants; recruitment and activation of neutrophils and macrophages cause tissue injury.

Clinical relevance: Immune complex–mediated diseases are collectively described as type III hypersensitivity. They include serum sickness, cryoglobulinemic vasculitis, post-infectious glomerulonephritis, lupus nephritis, and certain vasculitides.

Diagnosis and management: Diagnosis involves clinical history, signs of inflammation, low complement levels (C3, C4), and laboratory assays for circulating immune complexes (e.g., C1q-binding assays). Tissue biopsy can show immune complex deposition with immunofluorescence. Treatment targets the underlying cause and inflammation; plasmapheresis may be used in severe cases; corticosteroids and immunosuppressants may reduce immune complex formation and inflammation.