...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The journal of immunology >Regulatory B Cells (B10 Cells) and Regulatory T Cells Have Independent Roles in Controlling Experimental Autoimmune Encephalomyelitis Initiation and Late-Phase Immunopathogenesis
【24h】

Regulatory B Cells (B10 Cells) and Regulatory T Cells Have Independent Roles in Controlling Experimental Autoimmune Encephalomyelitis Initiation and Late-Phase Immunopathogenesis

机译：调节性B细胞（B10细胞）和调节性T细胞在控制实验性自身免疫性脑脊髓炎的启动和晚期免疫致病中具有独立的作用

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Experimental autoimmune encephalomyelitis (EAE) is a T lymphocyte-mediated autoimmune disease of the CNS. Significant roles for B cells and a rare IL-10–producing CD1dhighCD5+ regulatory B cell subset (B10 cells) have been identified during the initiation and progression of EAE. Whether and how the regulatory functions of B10 cells and FoxP3+ T regulatory cells (Tregs) overlap or influence EAE immunopathogenesis independently has remained unanswered. This study demonstrates that the number of endogenous or adoptively transferred B10 cells directly influenced EAE pathogenesis through their production of IL-10. B10 cell numbers expanded quickly within the spleen, but not CNS following myelin oligodendrocyte glycoprotein35–55 immunization, which paralleled B10 cell regulation of disease initiation. The adoptive transfer of myelin oligodendrocyte glycoprotein33–35-sensitized B10 cells into wild-type mice reduced EAE initiation dramatically. However, B10 cells did not suppress ongoing EAE disease. Rather, Treg numbers expanded significantly within the CNS during disease progression, which paralleled their negative regulation of late-phase disease. Likewise, the preferential depletion of B10 cells in vivo during disease initiation enhanced EAE pathogenesis, whereas Treg depletion enhanced late-phase disease. B10 cells did not regulate T cell proliferation during in vitro assays, but significantly altered CD4+ T cell IFN-γ and TNF-α production. Furthermore, B10 cells downregulated the ability of dendritic cells to act as APCs and thereby indirectly modulated T cell proliferation. Thus, B10 cells predominantly control disease initiation, whereas Tregs reciprocally inhibit late-phase disease, with overlapping B10 cell and Treg functions shaping the normal course of EAE immunopathogenesis.
机译：实验性自身免疫性脑脊髓炎（EAE）是T淋巴细胞介导的CNS自身免疫性疾病。在EAE的发生和发展过程中，已经确定了B细胞的重要作用以及罕见的产生IL-10的CD1dhighCD5 +调节性B细胞亚群（B10细胞）。 B10细胞和FoxP3 + T调节细胞（Tregs）的调节功能是否重叠以及如何相互独立或影响EAE免疫发病机制，尚无定论。这项研究表明，内源性或过继转移的B10细胞的数量通过产生IL-10直接影响EAE发病机理。髓鞘少突胶质细胞糖蛋白35-55免疫后，脾脏中的B10细胞数目迅速增加，但中枢神经系统却没有迅速增加，这与疾病发作的B10细胞调节平行。髓磷脂少突胶质细胞糖蛋白33–35敏感的B10细胞过继转移至野生型小鼠中可显着降低EAE的起始。但是，B10细胞不能抑制正在进行的EAE疾病。相反，在疾病进展过程中，CNS内的Treg数量显着增加，这与它们对晚期疾病的负面调节相一致。同样，疾病开始期间体内B10细胞的优先消耗增强了EAE发病机理，而Treg消耗则增强了晚期疾病。 B10细胞在体外测定过程中不调节T细胞增殖，但会显着改变CD4 + T细胞IFN-γ和TNF-α的产生。此外，B10细胞下调树突状细胞充当APC的能力，从而间接调节T细胞增殖。因此，B10细胞主要控制疾病的发生，而Tregs相互抑制晚期疾病，而B10细胞和Treg的功能重叠则形成了EAE免疫发病机制的正常过程。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号