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Mellanby, R.J., Cambrook, H., Turner, D.G., O’Connor, R.A., Leech, M.D., Kurschus, F.C., et al. (2012) TLR-4 Ligation of Dendritic Cells Is Sufficient to Drive Pathogenic T Cell Function in Experimental Autoimmune Encephalomyelitis. Journal of Neuroinflammation, 9, 248. http://dx.doi.org/10.1186/1742-2094-9-248

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

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

  KEYWORDS: IL10, B10, TLR4, CD40L, LPS

  JOURNAL NAME: Open Journal of Immunology, Vol.5 No.1, February 12, 2015

  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.