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Immune complex negatively regulates Toll‐like receptor 9‐mediated immune responses in B cells through the inhibitory Fc‐gamma receptor IIb
Author(s) -
Qian Li,
Chen Wenyan,
Qin Hongchao,
Rui Chenglei,
Jia Xiaoqin,
Fu Yi,
Gong Weijuan,
Tian Fang,
Ji Mingchun
Publication year - 2015
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12224
Subject(s) - tlr9 , cd80 , biology , immune system , toll like receptor 9 , toll like receptor , cd40 , receptor , immunology , microbiology and biotechnology , innate immune system , cytotoxic t cell , gene expression , in vitro , gene , biochemistry , dna methylation
Because inappropriate activation of Toll‐like receptor 9 (TLR9) may induce pathological damage, negative regulation of the TLR9‐triggered immune response has attracted considerable attention. Nonpathogenic immune complex (IC) has been demonstrated to have beneficial therapeutic effects in some kinds of autoimmune diseases. However, the role of IC in the regulation of TLR9‐triggered immune responses and the underlying mechanisms remain unclear. In this study, it was demonstrated that IC stimulation of B cells not only suppresses CpG‐oligodeoxynucleotide (CpG‐ODN)‐induced pro‐inflammatory IL‐6 and IgM κ production, but also attenuates CD40 and CD80 expression. Furthermore, our results suggest that the receptor for the Fc portion of IgG (FcγR) IIb is involved in the suppressive effect of IC on TLR9‐mediated CD40, CD80 and IL‐6 expression. Finally, it was found that IC down‐regulates TLR9 expression in CpG‐ODN activated B cells. Our results provide an outline of a new pathway for the negative regulation of TLR9‐triggered immune responses in B cells via FcγRIIb. A new mechanistic explanation of the therapeutic effect of nonpathogenic IC on inflammatory and autoimmune diseases is also provided.