Novel regulation of MHC class II function in B cells
Novel regulation of MHC class II function in B cells
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DOI：
10.1038/sj.emboj.7601556
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发表时间：
2007-02-07
期刊：
影响因子：
11.4
通讯作者：
Ishido, Satoshi
中科院分区：
文献类型：
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作者：
Matsuki, Yohei;Ohmura-Hoshino, Mari;Ishido, Satoshi
近年来，在具有抗原呈递细胞功能的树突状细胞（DC）中，已经证实了在生理条件下存在MHC II类分子（MHC II）的翻译后调节。在这里，我们报告，MARCH-I，E3泛素连接酶，在B细胞中的MHC II的翻译后调节中起着关键作用。MARCH-I在B细胞中表达特别高，并且MARCH-I的强制表达诱导MHC II的泛素化。在来自MARCH-1缺陷小鼠（MARCH-1 KO）的B细胞中，表面MHC II的半衰期延长，并且MHC II的泛素化形式完全消失。此外，MARCH-I缺陷型B细胞在其表面上高度表达负载外源抗原的MHC II，并显示出高的呈递外源抗原的能力。这些结果表明，MHC II在B细胞中的功能是通过MARCH-I的泛素化来调节的。
The presence of post-translational regulation of MHC class II ( MHC II) under physiological conditions has been demonstrated recently in dendritic cells (DCs) that potently function as antigen-presenting cells (APCs). Here, we report that MARCH-I, an E3 ubiquitin ligase, plays a pivotal role in the post-translational regulation of MHC II in B cells. MARCH-I expression was particularly high in B cells, and the forced expression of MARCH-I induced the ubiquitination of MHC II. In B cells from MARCH-I- deficient mice (MARCH-I KO), the half-life of surface MHC II was prolonged and the ubiquitinated form of MHC II completely disappeared. In addition, MARCH-I-deficient B cells highly expressed exogenous antigen-loaded MHC II on their surface and showed high ability to present exogenous antigens. These results suggest that the function of MHC II in B cells is regulated through ubiquitination by MARCH-I.