A 45-year-old man on infliximab for Crohn's disease develops fever, cough, and cavitary lung lesions. Sputum culture grows Mycobacterium tuberculosis. Which immunological mechanism explains this reactivation?

• A Inhibition of IL-17 signaling impairs mucosal immunity
• B Blockade of IL-2 receptor prevents T cell proliferation
• C Neutralization of TNF-alpha impairs granuloma formation and maintenance ✓
• D Inhibition of B cell maturation reduces opsonizing antibodies

Explanation

TNF-alpha is essential for formation and maintenance of granulomas that contain latent mycobacterial infections. Infliximab (anti-TNF-alpha monoclonal antibody) disrupts granuloma integrity, allowing reactivation of tuberculosis. This is a well-established adverse effect requiring TB screening before starting anti-TNF therapy. IL-17 inhibition affects mucocutaneous candidiasis. IL-2 receptor blockade is used in transplant. C cell depletion does not cause TB reactivation.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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