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首页> 外文期刊>Cytokine >MARCH1 down-regulation in IL-10-activated B cells increases MHC class II expression
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MARCH1 down-regulation in IL-10-activated B cells increases MHC class II expression

机译:IL-10-激活的B细胞中的MARCH1下调增加了MHC II类表达

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摘要

IL-10 is vastly studied for its anti-inflammatory properties on most immune cells. However, it has been reported that IL-10 activates B cells, up-regulates their MHC class II molecules and prevents apoptosis. As MARCH1 was shown to be responsible for the intracellular sequestration of MHC class II molecules in dendritic cells and monocytes in response to IL-10, we set out to clarify the role of this ubiquitin ligase in B cells. Here, we demonstrate in mice that splenic follicular B cells represent the major cell population that up-regulate MHC II molecules in the presence of IL-10. Activation of these cells through TLR4, CD40 or the IL-10 receptor caused the down-regulation of MARCH1 mRNA. Accordingly, B cells from MARCH1-deficient mice do not up-regulate I-A b in response to IL-10. In all, our results demonstrate that IL-10 can have opposite effects on MARCH1 regulation in different cell types.
机译:IL-10对大多数免疫细胞的抗炎特性已得到广泛研究。然而,据报道IL-10激活B细胞,上调其MHC II类分子并阻止细胞凋亡。由于显示MARCH1负责树突状细胞和单核细胞对IL-10的MHC II类分子的细胞内螯合,我们着手阐明这种泛素连接酶在B细胞中的作用。在这里,我们在小鼠中证明脾滤泡B细胞代表在IL-10存在下上调MHC II分子的主要细胞群。这些细胞通过TLR4,CD40或IL-10受体的激活导致MARCH1 mRNA的下调。因此,来自MARCH1缺陷型小鼠的B细胞不响应IL-10而上调I-A b。总之,我们的结果表明,IL-10在不同细胞类型中对MARCH1调控具有相反的作用。

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