脂多糖减弱小鼠脾细胞中CD40配体诱导的调节性B10细胞扩增及白细胞介素-10的产生。

Lipopolysaccharide Attenuates CD40 Ligand-Induced Regulatory B10 Cell Expansion and IL-10 Production in Mouse Splenocytes.

作者信息

Lin Mei, Lin Jiang, Wang Yuhua, Bonheur Nathalie, Kawai Toshihisa, Wang Zuomin, Han Xiaozhe

机构信息

Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, USA ; Department of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.

Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, USA ; Department of Stomatology, Fourth Hospital of Harbin Medical University, Harbin, China.

出版信息

Open J Immunol. 2015 Mar;5(1):1-8. doi: 10.4236/oji.2015.51001.

DOI:10.4236/oji.2015.51001

PMID:26236564

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4517687/

Abstract

Toll-like receptors (TLRs) play a key role in B cell-mediated innate and adaptive immunity. It has been shown that interleukin 10 (IL-10)-producing regulatory B cells (B10 cells) can negatively regulate cellular immune responses and inflammation in autoimmune diseases. In this study, we determined the effect of TLR4 signaling on the CD40-activated B10 cell competency. The results demonstrated that LPS and CD40L synergistically stimulated proliferation of mouse splenocytes. The percentage of B10 cells in cultured splenocytes was significantly increased after CD40L stimulation but such increase was diminished by the addition of LPS. Such effects by LPS were only observed in cells from WT but not TLR4 mice. IL-10 mRNA expression and protein production in B10 cells from cultured splenocytes were significantly up-regulated by CD40L stimulation but were inhibited after the addition of LPS in a TLR4-dependent manner. This study suggests that LPS-induced TLR4 signaling attenuate CD40L-activated regulatory B10 cell competency.

摘要

Toll样受体（TLRs）在B细胞介导的固有免疫和适应性免疫中起关键作用。研究表明，产生白细胞介素10（IL-10）的调节性B细胞（B10细胞）可在自身免疫性疾病中负向调节细胞免疫反应和炎症。在本研究中，我们确定了TLR4信号传导对CD40激活的B10细胞功能的影响。结果表明，脂多糖（LPS）和CD40配体（CD40L）协同刺激小鼠脾细胞增殖。CD40L刺激后，培养的脾细胞中B10细胞的百分比显著增加，但添加LPS后这种增加减弱。LPS的这种作用仅在野生型（WT）小鼠而非TLR4基因敲除小鼠的细胞中观察到。培养的脾细胞中B10细胞的IL-10信使核糖核酸（mRNA）表达和蛋白质产生在CD40L刺激后显著上调，但添加LPS后以TLR4依赖的方式受到抑制。本研究提示，LPS诱导的TLR4信号传导减弱了CD40L激活的调节性B10细胞功能。