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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 vitiligo is JAK mediated. Intrinsic and/or extrinsic factors induce the cellular stress response in melanocytes, which then activates innate immunity within the skin to trigger the initial inflammation that leads to autoimmunity. As a result, CXCL9 and CXCL10 are released from keratinocytes leading to recruitment of CD8⁺ T cells. Activated CD8⁺T cells produce IFNγ which trigger more CXCL9 and CXCL10 production from keratinocyte through JAK1 and JAK2 signaling and recruit more CD8⁺ T cells to the inflamed sites. CD8⁺ T cells then destruct melanocytes and lead to depigmentation. CXCL, chemokine (C-X-C motif) ligand; IFN, interferon; IL, interleukin; JAK, Janus kinase; NKD2D, natural killer group 2D.