In alopecia areata (AA), the inflammatory target is the hair bulb in the anagen phase. Which specific immune mechanism is responsible for breaking the immune privilege of the hair follicle?
- A IgG autoantibodies against follicular keratin
- B Upregulation of MHC class I and IFN-gamma signalling in follicular epithelium, enabling CD8+ T-cell attack ✓
- C NK cell-mediated cytotoxicity against follicular melanocytes
- D IL-4/IL-13 driven Th2 response causing eosinophilic folliculitis
Explanation
The normal anagen hair follicle maintains local immune privilege by downregulating MHC class I expression and producing immunosuppressive factors (TGF-beta, ACTH, MSH) that prevent T-cell recognition. In AA, IFN-gamma (from JAK1/JAK2 signalling) upregulates MHC class I on follicular epithelial cells, collapsing immune privilege and enabling autoreactive CD8+ T-cells to attack follicular antigens. This explains why JAK inhibitors (tofacitinib, baricitinib, ritlecitinib) are effective in AA.
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.