Describe Type III hypersensitivity mechanisms and give an example.

• A. Type III is mediated by T cell cytotoxicity.
• B. Type III arises from immune complex deposition in tissues, activating complement and inflammation (e.g., serum sickness, lupus nephritis).
• C. Type III is due to autoantibody production against thyroid hormones.
• D. Type III is mediated by IgE on mast cells.

Answer: (B)

Type III hypersensitivity is driven by immune complexes—antibody bound to soluble antigen—that circulate and deposit in tissues such as blood vessel walls and glomeruli. Once deposited, these complexes activate the classical complement pathway, producing inflammatory mediators like C3a and C5a. These attract and activate neutrophils, which release enzymes and reactive molecules that damage surrounding tissue, leading to inflammation and organ injury.

Classic examples include serum sickness, where repeated exposure to a foreign protein triggers circulating immune complexes and systemic inflammation, and lupus nephritis, where immune complexes deposit in the kidneys causing inflammation and impaired function.

This mechanism is distinct from T cell–mediated cytotoxicity (Type IV), antibody responses against hormones (not a typical description of a hypersensitivity type), and IgE-mediated mast cell degranulation (Type I). The described process—immune complex deposition with complement activation and ensuing inflammation—fits the described mechanism and examples.