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首页> 美国卫生研究院文献>Journal of Leukocyte Biology >Regulation of the mucosal phenotype in dendritic cells by PPARγ: role of tissue microenvironment
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Regulation of the mucosal phenotype in dendritic cells by PPARγ: role of tissue microenvironment

机译：PPARγ对树突状细胞黏膜表型的调节：组织微环境的作用

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Mucosal DCs play a critical role in tissue homeostasis. Several stimuli can induce a mucosal phenotype; however, molecular pathways that regulate development of mucosal DC function are relatively unknown. This study sought to determine whether PPARγ contributes to the development of the “mucosal” phenotype in mouse DCs. Experiments demonstrated that PPARγ activation in BMDCs induced an immunosuppressive phenotype in which BMDCs had reduced expression of MHC class II and costimulatory molecules, increased IL-10 secretion, and reduced the ability to induce CD4 T cell proliferation. Activation of PPARγ enhanced the ability of BMDC to polarize CD4 T cells toward iTregs and to induce T cell expression of the mucosal homing receptor, CCR9. Activation of PPARγ increased the ability of BMDCs to induce T cell-independent IgA production in B cells. BMDCs from PPARγΔDC mice displayed enhanced expression of costimulatory molecules, enhanced proinflammatory cytokine production, and decreased IL-10 synthesis. Contrary to the inflammatory BMDC phenotype in vitro, PPARγΔDC mice showed no change in the frequency or phenotype of mDC in the colon. In contrast, mDCs in the lungs were increased significantly in PPARγΔDC mice. A modest increase in colitis severity was observed in DSS-treated PPARγΔDC mice compared with control. These results indicate that PPARγ activation induces a mucosal phenotype in mDCs and that loss of PPARγ promotes an inflammatory phenotype. However, the intestinal microenvironment in vivo can maintain the mucosal DC phenotype of via PPARγ-independent mechanisms.
机译：粘膜DC在组织动态平衡中起关键作用。几种刺激可以诱导粘膜表型。然而，调节粘膜DC功能发展的分子途径相对未知。这项研究试图确定PPARγ是否有助于小鼠DC中“粘膜”表型的发展。实验表明，BMDCs中的PPARγ激活诱导了免疫抑制表型，其中BMDCs降低了II类MHC和共刺激分子的表达，增加了IL-10的分泌，并降低了诱导CD4 T细胞增殖的能力。 PPARγ的激活增强了BMDC使CD4 T细胞朝iTreg极化并诱导粘膜归巢受体CCR9 T细胞表达的能力。 PPARγ的激活增加了BMDC诱导B细胞中独立于T细胞的IgA产生的能力。 PPARγΔDC小鼠的BMDC表现出共刺激分子表达增强，促炎细胞因子产生增加，IL-10合成减少。与体外炎症性BMDC表型相反，PPARγΔDC小鼠结肠中mDC的频率或表型没有变化。相反，PPARγΔDC小鼠的肺中mDCs显着增加。与对照组相比，在经DSS处理的PPARγΔDC小鼠中，结肠炎严重程度有所增加。这些结果表明，PPARγ活化在mDC中诱导了粘膜表型，并且PPARγ的丧失促进了炎性表型。然而，体内的肠道微环境可以通过不依赖PPARγ的机制维持黏膜DC表型。

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