Abstract
Among interleukin (IL)‐17 family, IL‐17A and IL‐17F share amino acid sequence similarity and IL‐17 receptor type A. IL‐17 signaling is implicated in the pathogenesis of various autoimmune diseases, but its role in the regulatory mechanism of extracellular matrix (ECM) expression remains to be elucidated. We found that dermal fibroblasts express type A receptor for IL‐17. We then determined whether IL‐17 affects ECM expression in dermal fibroblasts.The cDNA array of ECM genes and Immunoblot showed IL‐17A, not IL‐17F, reduced the expression of connective tissue growth factor (CTGF) as well as α1(I) collagen. miR‐129–5p increased by IL‐17A and mediated the α1(I) collagen reduction. These results suggest that IL‐17A signaling, not IL‐17F, has an anti‐fibrogenic effect via the up‐regulation of miR‐129–5p and the down‐regulation of CTGF and α1(I) collagen. Expression of IL‐17 receptor in cultured dermal fibroblasts derived from patients with scleroderma, one of the fibrotic skin diseases, was significantly down‐regulated, which may contribute to the tissue fibrosis.IL‐17A may play important roles in tissue remodeling of the skin. Clarifying the novel regulatory mechanisms of tissue remodeling by IL‐17A signal may lead to a new therapeutic approach against various skin diseases with connective tissue abnormalities.
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