STAT3 but not STAT4 is critical for γδT17 cell responses and skin inflammation.

The transcription factors and are essential for lymphocyte differentiation and function. Interleukin (IL)-17 producing γδ T (γδT17) cells are innate lymphocytes important for anti-bacterial and inflammatory responses at barrier surfaces. Herein, we examine the role of duanyu18133 and duanyu18134 in regulating the homeostasis, activation, and pathogenicity of γδT17 cells. We show that duanyu18133 sustains γδT17 numbers in the skin but not in the lymph nodes, while duanyu18134 deficiency does not affect their homeostasis. Similarly, duanyu18133 but not duanyu18134 is essential for IL-23-induced IL-22 production by γδT17 cells. Concomitantly, mice lacking duanyu18133 expression in γδT17 cells develop significantly reduced psoriasis-like inflammation. γδT17 cells fail to expand and to upregulate IL-17A, IL-17F, and IL-22 in response to psoriatic stimuli. Although animals develop psoriasis-like disease, γδT17 cells in these mice are defective in IL-17F production. Collectively, our data demonstrate for the first time a critical role for duanyu18133 in orchestrating the homeostasis and pathogenicity of γδT17 cells and provide evidence for the requirement of duanyu18134 for optimal cytokine responses during inflammation. © 2019 The Authors.

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