A patient with active vitiligo has autoantibodies detected in her serum. The primary mechanism of melanocyte destruction in vitiligo is best characterized by:

• A CD8+ cytotoxic T lymphocytes and innate immunity (IFN-γ/CXCL10 axis) targeting melanocyte-specific antigens ✓
• B Type II hypersensitivity — IgG antibodies directly lysing melanocytes via complement
• C IgE-mediated mast cell degranulation damaging melanocytes
• D Neutrophil-mediated oxidative damage from hydrogen peroxide accumulation

Explanation

Current evidence strongly supports that CD8+ cytotoxic T lymphocytes (CTLs) are the primary effectors of melanocyte destruction in vitiligo. IFN-γ released by CTLs drives keratinocyte production of CXCL9 and CXCL10, recruiting more CD8+ T cells via CXCR3 (IFN-γ/CXCL10 feedback loop). Melanocyte-specific antigens include Melan-A/MART-1 and tyrosinase. This understanding has led to the JAK1/2 inhibitor ruxolitinib being FDA-approved for vitiligo by blocking JAK-STAT signalling downstream of IFN-γ.

Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.