In Type III hypersensitivity (immune complex-mediated), the key complement-derived factor responsible for neutrophil recruitment to sites of immune complex deposition is:
- A C3b (acting as opsonin)
- B C4a (weak anaphylatoxin)
- C C5a (potent anaphylatoxin and neutrophil chemoattractant) ✓
- D C1q (initiating classical pathway activation)
Explanation
In serum sickness and Arthus reaction (Type III hypersensitivity), immune complexes deposited in vessel walls activate complement via the classical pathway. The most biologically important product is C5a: it acts as a potent chemoattractant (drawing neutrophils to the deposits) and as an anaphylatoxin (activating mast cells to release vasoactive amines). Neutrophils then release proteases and reactive oxygen species, causing tissue damage (vasculitis). C3b is an opsonin for phagocytosis. C4a is a weak anaphylatoxin with minimal in vivo significance. C1q initiates the pathway but is not directly responsible for neutrophil recruitment.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.