Loss of CD103 reduces chronic inflammation by decreasing the retention of IL-17a-secreting γδ T cells in mouse model of psoriasis

Summary: CD103-positive γδ T cells accumulate in psoriasis-like inflamed skin and serve as a major source of IL-17A, leading to Th1/Th17-mediated inflammation. The study investigates the role of CD103 in regulating IL-17A-secreting γδ T cells and its impact on chronic inflammation. Using a K14CreER-Ube2l3f/f mouse model simulating psoriatic dermatitis and a CD103-deficient mouse model, we evaluated the infiltration and persistence of γδ T cells in inflammatory tissue and the expression of CD103 by flow cytometry and immunofluorescence. Our results demonstrate that CD103 deficiency significantly reduces the population of tissue-resident γδ T cells secreting IL-17A compared to wild-type controls (p < 0.01). The absence of CD103 impairs the ability of γδ T cells to secrete IL-17A, weakens their adhesion to epithelial cells, and limits their retention in inflammatory tissue. These findings highlight CD103 as a key regulator of γδ T cell retention and chronic inflammation. Liran Ye¹ 1. Zhejiang University, Hangzhou, Zhejiang, China. Innate Immunity, Microbiology, and Microbiome