Cyclosporin regulates TGF-beta expression of intestinal mucosa by regulatory T cells

环孢素（CsA）在溃疡性结肠炎的治疗中表现出快速的改善，但其确切的机制尚不清楚。我们假设CsA会影响肠黏膜tgf - β的表达。在CD4+CD25+细胞转移的SCID小鼠中，给予4% DSS诱导结肠炎。CsA治疗通过减少上皮细胞凋亡改善粘膜破坏。CsA上调结肠中的tgf - β。在SCID小鼠中，tgf - β的表达被显著抑制，CsA处理不能上调tgf - β的表达。另一方面，CsA处理可上调CD4+CD25+细胞转移的SCID小鼠的tgf - β表达。然而，体外CsA处理并未增加分离的cd4 +CD25+细胞的tgf - β生成。这些结果表明，CsA治疗可以通过tgf - β相关途径改善上皮损伤。CD4+CD25+T细胞通过tgf - β相关途径间接介导CsA的保护作用。

Cyclosporine (CsA) showed a rapid improvement in the treatment of ulcerative colitis, but the precise mechanism is still obscure. We hypothesized that CsA would affect the TGF-beta expression of intestinal mucosa. Colitis was induced by feeding of 4% DSS in CD4+CD25+cells-transferred SCID mice. Treatment of CsA ameliorated mucosal destruction through reduction of epithelial apoptosis. CsA up-regulated the TGF-beta in the colon. TGF-beta expression was significantly suppressed and treatment of CsA failed to up-regulate the expression of TGF-beta in SCID mice. On the other hand, treatment of CsA up-regulated TGF-beta expression in CD4+CD25+cells-transferred SCID mice. However, TGF-beta production from separated-CD4+CD25+cells was not increased by treatment of CsA in vitro. These results demonstrate that treatment of CsA can ameliorate epithelial damage through TGF-beta-related pathway. CD4+CD25+T cells would indirectly mediate the protective effect of CsA via TGF-beta-related pathway.