Wang, JocelynPajulas, AbigailFu, YongyaoAdom , DjamilatouZhang, WenwuNelson, Andrew S.Spandau, Dan F.Kaplan, Mark H.2024-06-102024-06-102022-10Wang, J., Pajulas, A., Fu, Y., Adom, D., Zhang, W., Nelson, A. S., Spandau, D. F., & Kaplan, M. H. (2022). Γδ T Cell‒Mediated Wound Healing Is Diminished by Allergic Skin Inflammation. Journal of Investigative Dermatology, 142(10), 2805-2816.e4. https://doi.org/10.1016/j.jid.2022.03.012https://hdl.handle.net/1805/41338Atopic dermatitis results in profound changes in the function of the skin that include diminished barrier function and altered production of antimicrobial peptides. Our previous work in a model of allergic skin inflammation identified a defect in the wound healing process that was dependent on IL-4. In this report, we show that allergic skin inflammation results in a dramatic decrease in the presence of the Vγ3+ dendritic epidermal T-cell (DETC) population of γδ T cells in the skin. In mice that express an active signal transducer and activator of transcription 6 in T cells, DETCs are lost early in life. The loss of DETCs is entirely dependent on IL-4 and is recovered with a genetic deficiency of IL-4. Moreover, injection of IL-4 into wild-type mice results in acute loss of the DETC population. A similar loss of DETCs was observed in mice treated topically with MC903. Wounding of skin from Stat6VT-transgenic or MC903-treated mice resulted in decreased production of DETC-dependent cytokines in the skin, coincident with diminished wound closure. Importantly, intradermal injection of the DETC-produced cytokine fibroblast GF 7 rescued the rate of wound closure in mice with allergic skin inflammation. Together, these results suggest that the atopic environment diminishes prohealing T-cell populations in the skin, resulting in attenuated wound healing responses.en-USPublisher PolicyAtopic dermatitisAntimicrobial peptidesSkin inflammationγδ T cellsArticle