In non-segmental vitiligo, the autoimmune destruction of melanocytes is primarily mediated by:

• A B-cell autoantibodies against melanocyte surface antigens
• B CD8+ cytotoxic T-lymphocytes specific for melanocyte antigens (melanocyte-specific CTLs) ✓
• C Complement-mediated lysis via anti-melanocyte IgM
• D NK cell activity driven by absent MHC-I on melanocytes

Explanation

Current evidence strongly implicates autoreactive CD8+ cytotoxic T-lymphocytes (CTLs) as the primary effectors of melanocyte destruction in non-segmental vitiligo. These CTLs recognise melanocyte-specific antigens (MART-1/Melan-A, tyrosinase, gp100) presented on MHC-I. The JAK-STAT pathway (particularly IFN-gamma–CXCL9/CXCL10 axis) recruits these CTLs to the skin. This explains the efficacy of ruxolitinib cream (JAK1/2 inhibitor), the first FDA-approved topical treatment for vitiligo. Autoantibodies exist but play a secondary/unclear role; complement lysis and NK cells are not the primary mechanism.

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.