炎性细胞因子如白细胞介素-17 (il-17)可促进炎性自身免疫性疾病

Inflammatory cytokines such as interleukin -17 (il-17) promotes an inflammatory autoimmune disease. Although studies have shown that, mirnas to regulate the pathogenesis of autoimmunity through the development and function of lymphocytes, but its role in the inflammatory lesion is not clear. Here, we find mir-23b lupus or rheumatoid arthritis and a reduction in inflammatory lesions in lupus, rheumatoid arthritis or multiple sclerosis in a mouse model. Il-17 down-regulated human fibroblast-like synovial cells, mouse kidney cells and primary astrocytes expressing mir-23b and mir-23b down play an important role in the autoimmune mechanism. Conversely, mir-23b inhibition of il-17, tumor necrosis factor -α (tnf) for tgf-beta-activated kinase 1 / map3k7 binding protein 2 (tab2) tab3, and nuclear factor kappa-b α subunit kinase (IKKa) [alpha) or il-1β induced activation and nf-kappab expression of inflammatory cytokines, thus inhibiting autoimmunity. Inflammation. Thus, il-17 by inhibiting the expression of mir-23b radioactive cells, promote the expression of proinflammatory cytokines involved in autoimmune pathogenesis.

Inflammatory cytokines such as leukocyte interleukin-17 (il-17) promote inflammatory autoimmune diseases. Although studies have shown that mirnas regulate the pathogenesis of autoimmune by affecting the development and function of lymphocytes, their role in inflammatory damage is not clear. Here, we found that mir-23b was lowered in inflammatory lesions of lupus or rheumatoid arthritis, as well as in mouse models of lupus, rheumatoid arthritis, or multiple sclerosis. Il-17 lowers the expression of human fibroblast-like sliding membrane cells, mouse primary renal cells and star cell mir-23b, and lowers mir-23b in the autoimmune mechanism. In turn, mir-23b inhibits il-17, tumor necrosis factor-alpha (tnf) for tgf-beta-aradicalkinase 1 / map3k7 binding protein 2 (tab2) tab3, and nuclear factor kappa-b kinase alpha sub-base (ialphakk)-alpha) or il-1 beta induces nf-kappab activation and expression of inflammatory cytokines to suppress autoimmune. Inflammation. Therefore, il-17 promotes the expression of pro-inflammatory cytokines by inhibiting the expression of mir-23b in radioactive cells, and participates in the autoimmune pathogenesis.

Inflammatory cytokines such as interleukin-17 (IL-17) can promote inflammatory autoimmune diseases. Although some studies have shown that miRNAs regulate the pathogenesis of autoimmunity by affecting the development and function of lymphocyte, its role in inflammation injury is still unclear. Here, we found that mir-23b was down-regulated in inflammatory lesions of lupus or rheumatoid arthritis and in mice models of lupus, rheumatoid arthritis or multiple sclerosis. Il-17 down-regulates the expression of mir-23b in human fibroblast-like synovial cells, primary kidney cells and astrocytes, and plays an important role in the autoimmune mechanism. In turn, mir-23b inhibits il-17, tumor necrosis factor-alpha (tnf) targeting tgf-beta-activated kinase 1/map3k7 binding protein 2 (tab2) tab3, and nuclear factor kappa-B kinase alpha subunit (ikkalpha) - alpha or il-1bet inducing NF-kappaB activation and inflammatory cytokine expression, thereby inhibiting autoimmunity. Inflammation. Therefore, IL-17 promotes the expression of pro-inflammatory cytokines by inhibiting the expression of mir-23b in radiation cells and participates in the pathogenesis of autoimmunity.<br>