In serum sickness (type III hypersensitivity), the immune complex deposition at vessel walls activates complement. Which complement fragment generated during this process is most responsible for mast cell degranulation and increased vascular permeability?

• A C3b (opsonin)
• B C3a and C5a (anaphylatoxins) ✓
• C C1q (initiator of classical pathway)
• D C4a (weak anaphylatoxin — not the primary mediator)

Explanation

C3a and C5a are anaphylatoxins generated when complement is activated by immune complexes (classical pathway or alternative pathway amplification). They bind C3aR and C5aR1 on mast cells and basophils, triggering degranulation with histamine release, causing increased vascular permeability and smooth muscle contraction. C5a is additionally a potent neutrophil chemoattractant driving the vasculitis of serum sickness. C3b is a critical opsonin for phagocytosis. C4a is a weak anaphylatoxin with minimal physiological effect compared to C3a/C5a.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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