A regulatory B cell subset with a unique CD1dhiCD5+ phenotype controls T cell-dependent inflammatory responses
A regulatory B cell subset with a unique CD1dhiCD5+ phenotype controls T cell-dependent inflammatory responses
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DOI：
10.1016/j.immuni.2008.03.017
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发表时间：
2008-05-01
期刊：
影响因子：
32.4
通讯作者：
Tedder, Thomas F.
中科院分区：
文献类型：
--
作者：
Yanaba, Koichi;Bouaziz, Jean-David;Tedder, Thomas F.
B细胞介导多种影响免疫和炎症反应的功能。在这项研究中，T细胞介导的炎症在Cd19缺陷（Cd19(-/-)）小鼠和CD20(+) B细胞缺失的野生型小鼠中被夸大，而在B细胞过度活跃的小鼠中，由于Cd19过表达（hCD19Tg），炎症大大减少。这些炎症反应受到Cd19（-/-）小鼠中不存在的独特的CD1d(hi)CD5(+) B细胞亚群的负调控，在野生型小鼠中仅占脾脏B220（+）细胞的1%-2%，但在hCD19Tg小鼠中扩展到脾脏B220（+）细胞的10%左右。在CD20+ B细胞缺失的野生型小鼠和Cd19（-/-）小鼠中，这些CD1d(hi)CD5(+) B细胞的过继转移使炎症正常化。值得注意的是，IL-10的产生仅限于CD1d(hi)CD5(+) B细胞亚群，在Cd19（-/-）小鼠中IL-10的产生减少，而在hCD19Tg小鼠中IL-10的产生增加。因此，CD1d(hi)CD5(+) B细胞代表了一种独特的有效调节性B细胞亚群。
B cells mediate multiple functions that influence immune and inflammatory responses. In this study, T cell-mediated inflammation was exaggerated in CD19-deficient (Cd19(-/-)) mice and wild-type mice depleted of CD20(+) B cells, whereas inflammation was substantially reduced in mice with hyperactive B cells as a result of CD19 overexpression (hCD19Tg). These inflammatory responses were negatively regulated by a unique CD1d(hi)CD5(+) B cell subset that was absent in Cd19(-/-) mice, represented only 1%-2% of spleen B220(+) cells in wild-type mice, but was expanded to similar to 10% of spleen B220(+) cells in hCD19Tg mice. Adoptive transfer of these CD1d(hi)CD5(+) B cells normalized inflammation in wild-type mice depleted of CD20+ B cells and in Cd19(-/-) mice. Remarkably, IL-10 production was restricted to this CD1d(hi)CD5(+) B cell subset, with IL-10 production diminished in Cd19(-/-) mice, yet increased in hCD19Tg mice. Thereby, CD1d(hi)CD5(+) B cells represent a unique subset of potent regulatory B cells.