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

Mei Lin^1,2, Jiang Lin^1,3, Yuhua Wang^1,4, Nathalie Bonheur¹, Toshihisa Kawai¹, Zuomin Wang^2*, Xiaozhe Han^1*

¹Department of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, USA.
²Department of Stomatology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
³Department of Stomatology, Fourth Hospital of Harbin Medical University, Harbin, China.
⁴Department of Stomatology, Shanghai 9th People’s Hospital, Shanghai, China.

DOI: 10.4236/oji.2015.51001                

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.

Keywords

IL10, B10, TLR4, CD40L, LPS

Conflicts of Interest

The authors declare no conflicts of interest.

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