immunecomplex

Immune complexes are aggregates that form when antibodies bind soluble antigens. The resulting complexes can be soluble and circulating or become deposited as insoluble structures in tissues.

Formation of immune complexes depends on the antigen-to-antibody ratio, with a zone of equivalence in which lattice-like assemblies form most readily. Soluble immune complexes can circulate in the bloodstream; if not cleared efficiently, they may deposit in vascular walls, joints, or organs such as the kidneys.

In circulation, immune complexes can activate the classical complement pathway via C1q binding, leading to generation of inflammatory mediators such as C3a and C5a. Complement deposition promotes recruitment of neutrophils and other inflammatory cells and opsonization by C3b, facilitating phagocytosis. Tissue deposition of immune complexes can trigger type III hypersensitivity reactions, causing vasculitis, glomerulonephritis, and other inflammatory processes.

Clinically, immune complex–mediated diseases include serum sickness, post-infectious glomerulonephritis, systemic lupus erythematosus–related manifestations, cryoglobulinemic vasculitis, and rheumatoid arthritis–associated vasculitis. Symptoms often reflect the affected sites and may include fever, rash, arthralgia, and nephritis.

Diagnosis relies on clinical presentation supported by laboratory findings such as reduced complement levels and, in some cases, assays that detect circulating immune complexes. Management targets the underlying antigen source and inflammation, with options including anti-inflammatory therapy, immunosuppression, and plasmapheresis in selected severe cases.