Which type of hypersensitivity is characterized by immune complexes deposited in small blood vessels?

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Multiple Choice

Which type of hypersensitivity is characterized by immune complexes deposited in small blood vessels?

Explanation:
Immune complex–mediated hypersensitivity is driven by the formation of antigen–antibody complexes that circulate and deposit in tissues, especially in small blood vessels. When these complexes lodge in vessel walls, they activate the complement system, producing inflammatory traffic signals (like C3a and C5a) that recruit neutrophils. The neutrophils release enzymes and reactive species that damage the vessel walls, leading to vasculitis and tissue injury. This pattern—immune complexes in small vessels with complement activation and neutrophil-driven inflammation—defines this type and explains manifestations such as serum sickness–like symptoms and vasculitic rashes. In contrast, immediate hypersensitivity is mediated by IgE on mast cells causing rapid allergic reactions, cytotoxic hypersensitivity involves antibodies targeting cell surfaces leading to cell destruction, and delayed-type hypersensitivity is driven by T cells rather than antibodies and immune complexes.

Immune complex–mediated hypersensitivity is driven by the formation of antigen–antibody complexes that circulate and deposit in tissues, especially in small blood vessels. When these complexes lodge in vessel walls, they activate the complement system, producing inflammatory traffic signals (like C3a and C5a) that recruit neutrophils. The neutrophils release enzymes and reactive species that damage the vessel walls, leading to vasculitis and tissue injury. This pattern—immune complexes in small vessels with complement activation and neutrophil-driven inflammation—defines this type and explains manifestations such as serum sickness–like symptoms and vasculitic rashes.

In contrast, immediate hypersensitivity is mediated by IgE on mast cells causing rapid allergic reactions, cytotoxic hypersensitivity involves antibodies targeting cell surfaces leading to cell destruction, and delayed-type hypersensitivity is driven by T cells rather than antibodies and immune complexes.

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