Vogt-Koyanagi-Harada (VKH) disease involves autoimmune attack on melanocyte-containing tissues. Which immunopathological mechanism is primarily responsible?
- A CD4+ T-cell (Th1) response against melanocyte-associated antigens (tyrosinase, gp100) ✓
- B B-cell-mediated antibody production against melanocyte surface antigens
- C Molecular mimicry between infectious agents and uveal melanocytes
- D Complement activation via classical pathway on choroidal vessels
Explanation
VKH disease is a T-cell-mediated (Th1/Th17) autoimmune disorder targeting melanocyte-associated antigens, particularly tyrosinase and other melanosomal proteins. Activated CD4+ T helper cells sensitised to melanocyte antigens infiltrate melanocyte-containing tissues: uvea, meninges, inner ear, and skin. This explains the multi-system involvement: uveitis, aseptic meningitis (headache, stiff neck), sensorineural hearing loss/tinnitus, and alopecia/vitiligo/poliosis (sunset glow fundus, Dalen-Fuchs nodules). HLA-DR4 (specifically DRB1*04:05) is the dominant genetic association. High-dose systemic corticosteroids are the cornerstone of treatment.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
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Written and medically reviewed by the StethoPrep medical team.