A 70-year-old woman develops jaw claudication and sudden vision loss. ESR 95 mm/h. Temporal artery biopsy shows granulomatous inflammation with giant cells and fragmentation of the internal elastic lamina. The primary cellular mediator driving this vasculitis is:

• A CD8+ cytotoxic T cells releasing granzyme B into endothelium
• B Neutrophil degranulation with release of MPO and elastase
• C B cell-produced ANCA activating neutrophils
• D CD4+ Th1 cells producing IFN-gamma driving macrophage activation and granuloma formation ✓

Explanation

Giant cell arteritis (temporal arteritis) is a CD4+ Th1-mediated granulomatous large vessel vasculitis. Activated CD4+ T cells recognize arterial wall antigens, producing IFN-gamma that drives macrophage activation, giant cell formation, and fragmentation of the internal elastic lamina. Elevated IL-6 accounts for systemic symptoms and high ESR. ANCA-associated vasculitides (GPA, MPA, EGPA) involve neutrophil activation by ANCA; CD8+ T cells are relevant in viral vasculitis.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.