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. 2018 Apr 25;9:883. doi: 10.3389/fimmu.2018.00883

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Copyright © 2018 Sharma and Rudra.

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 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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Cutaneous regulatory T-cells (Tregs) actively repair skin tissue damage. Tregs migrate to skin by virtue of sequential interactions of chemokines CCL17 and CCL22 with their receptor CCR4. CCL17 is secreted by endothelial cells in inflamed skin and helps in extravasation of Tregs, CCL22 manages subsequent migration of Tregs. In case of skin wound-induced inflammation, Tregs acquire a highly activated phenotype with higher surface expression of CTLA4 and ICOS. These Tregs actively suppress IFNγ production from inflammatory Ly6C⁺ macrophages. Also, Tregs express high amount of EGFR, helping in their tissue repair ability. In case of short wave UVB light induced skin damage, self mRNA from keratinocytes are taken up by CD103⁺ dendritic cells (DCs) which induce the cutaneous inflammation. These DCs are suppressed by Tregs which have high surface expression of CD103 and P-lig and thus can migrate into non-inflamed skin as well, subsequent to UV exposure.