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The immune complex deposition pathway refers to the formation of soluble antigen-antibody complexes (ICs), typically involving IgG or IgM, which circulate and deposit in tissues when clearance mechanisms are overwhelmed or impaired. Once deposited, ICs activate the classical pathway of the complement system—initiated by C1q binding—resulting in recruitment of neutrophils and other inflammatory cells, opsonization, and direct tissue injury. This mechanism is central to the pathogenesis of various autoimmune and inflammatory diseases, most notably systemic lupus erythematosus, rheumatoid arthritis, and glomerulonephritis. Key molecular players include complement proteins (C1q, C3, C5), Fcγ receptors on innate immune cells, cytokines, and chemokines. Therapeutic approaches target these molecules to prevent or limit immune complex-mediated tissue damage, but direct targeting of the "immune complex deposition pathway" is not possible, as it is not a discrete entity but a cascade of immune events.
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