MARCH1 down-regulation in IL-10-activated B cells increases MHC class II expression
MARCH1 down-regulation in IL-10-activated B cells increases MHC class II expression
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DOI：
10.1016/j.cyto.2012.03.015
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发表时间：
2012-07-01
期刊：
影响因子：
3.8
通讯作者：
Thibodeau, Jacques
中科院分区：
文献类型：
--
作者：
Galbas, Tristan;Steimle, Viktor;Thibodeau, Jacques
IL-10因其对大多数免疫细胞的抗炎特性而被广泛研究。然而，据报道，IL-10激活B细胞，上调其MHC II类分子并防止细胞凋亡。由于MARCH 1被证明是负责在树突状细胞和单核细胞响应IL-10的MHC II类分子的细胞内隔离，我们着手阐明这种泛素连接酶在B细胞中的作用。在这里，我们证明了在小鼠脾滤泡B细胞代表的主要细胞群，上调MHC II分子在IL-10的存在。通过TLR 4、CD 40或IL-10受体激活这些细胞导致MARCH 1 mRNA下调。因此，来自MARCH 1缺陷小鼠的B细胞不响应IL-10上调I-A（B）。总之，我们的研究结果表明，IL-10可以在不同的细胞类型中对MARCH 1调节产生相反的影响。(C)2012爱思唯尔有限公司保留所有权利。
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. (C) 2012 Elsevier Ltd. All rights reserved.