Vγ4 T Cells Inhibit the Pro-healing Functions of Dendritic Epidermal T Cells to Delay Skin Wound Closure Through IL-17A.

Abstract:

:Dendritic epidermal T cells (DETCs) and dermal Vγ4 T cells engage in wound re-epithelialization and skin inflammation. However, it remains unknown whether a functional link between Vγ4 T cell pro-inflammation and DETC pro-healing exists to affect the outcome of skin wound closure. Here, we revealed that Vγ4 T cell-derived IL-17A inhibited IGF-1 production by DETCs to delay skin wound healing. Epidermal IL-1β and IL-23 were required for Vγ4 T cells to suppress IGF-1 production by DETCs after skin injury. Moreover, we clarified that IL-1β rather than IL-23 played a more important role in inhibiting IGF-1 production by DETCs in an NF-κB-dependent manner. Together, these findings suggested a mechanistic link between Vγ4 T cell-derived IL-17A, epidermal IL-1β/IL-23, DETC-derived IGF-1, and wound-healing responses in the skin.

journal_name

Front Immunol

journal_title

Frontiers in immunology

authors

Li Y,Wang Y,Zhou L,Liu M,Liang G,Yan R,Jiang Y,Hao J,Zhang X,Hu X,Huang Y,Wang R,Yin Z,Wu J,Luo G,He W

doi

10.3389/fimmu.2018.00240

subject

Has Abstract

pub_date

2018-02-12 00:00:00

pages

240

issn

1664-3224

journal_volume

9

pub_type

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