Abstract
Psoriasis is a common chronic inflammatory and T cell-meditated skin disease. Runt-related transcription factor 3 (RUNX3), one of the runt-domain family of transcription factors, has been reported to be a susceptibility gene for psoriasis. The present study was designed to delineate the role and underlying mechanism of RUNX3 involved in the differentiation of T helper (Th) 17 and Th22 cells in psoriasis. The results of the present study demonstrated that the expression of RUNX3 increased significantly in CD4-positive (CD4+) T cells from patients with psoriasis, compared with healthy controls. In addition, increased levels of interleukin (IL)-6, IL-20 and IL-22, and increased frequencies of Th17 and Th22 cells were found in the patients with psoriasis patients, compared with the healthy controls. It was also found that the overexpression of RUNX3 increased the levels of Th17- and Th22-associated cytokines in the CD4+ T cells from the healthy controls. However, the inhibition of RUNX3 reduced the levels of the associated cytokines and decreased the frequency of Th17 and Th22 cells in the CD4+ T cells from the patients with psoriasis. Taken together, the present study suggested that RUNX3 regulated the differentiation of Th17 and Th22 cells in psoriasis, providing a promising therapeutic strategy for the treatment of psoriasis.
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