Abstract

Alopecia areata (AA) is an immune-mediated hair follicle (HF) disorder induced by elevated IFNγ levels and a Tc1-driven inflammatory response. We have previously shown that treatment with IL-12 and IL-18 induces IFNγ-dependent, immune privilege collapse of the hair bulb, which can be inhibited by blocking IL-12 receptor signaling with the TYK2 inhibitor, BMS-986202 (BMS), in human microdissected HFs. Here, we further investigate the role of TYK2 and its inhibition in AA pathogenesis. We cultured human full thickness non-lesional and lesional scalp skin biopsies from acute or chronic AA patients ex vivo with BMS.

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