NBME Immunology Practice Test 2026 – Complete Exam Prep

Immune complex–mediated tissue injury is driven by circulating antigen–antibody complexes that deposit in tissues such as vessel walls or glomeruli. Once deposited, these complexes activate the classical complement pathway, generating inflammatory mediators like C3a and C5a that recruit and activate neutrophils, leading to inflammation and local damage. This pattern of tissue injury is the hallmark of a Type III hypersensitivity reaction. Examples include serum sickness and the Arthus reaction, where immune complexes drive inflammation in tissues.

The other hypersensitivity types involve different mechanisms. Type I is driven by IgE and mast cell degranulation causing an immediate allergic response. Type II involves antibodies binding to cell-surface or extracellular matrix antigens, leading to cytotoxic effects or opsonization rather than immune complex deposition. Type IV is T-cell–mediated delayed-type hypersensitivity, with macrophage activation and granuloma formation rather than antibody-driven immune complex deposition.