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. 2019 Oct 9;10:2342. doi: 10.3389/fimmu.2019.02342

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Copyright © 2019 Howell, Kuo and Smith.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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IFNγ-driven inflammation in alopecia areata is JAK mediated. CD8⁺ T cells infiltrate the dermis, localize to the hair follicle bulb, and release IFNγ. IFNγ binds the IFN receptor on the surface of the follicular epithelial cell, which in turn signals via JAK1 and JAK2 to promote production of IL-15, a mediator of CD8⁺ T-cell activation. IL-15 binds IL-15 receptor on the CD8⁺ T cell surface, resulting in signaling via JAK1 and JAK3 to enhance the production of IFNγ and amplify the feedback loop. CD8⁺ T cells then attack the hair follicle, which causes hair loss. CXCL, chemokine (C-X-C motif) ligand; IFN, interferon; JAK, Janus kinase.