TLR signaling in B-cell development and activation

被引:203
作者
Hua, Zhaolin [1 ]
Hou, Baidong [1 ]
机构
[1] Chinese Acad Sci, Inst Biophys, Key Lab Infect & Immun, Beijing 100080, Peoples R China
基金
中国国家自然科学基金;
关键词
autoimmunity; B-cell development; germinal center; Toll-like receptor; TOLL-LIKE RECEPTORS; CLASS-SWITCH RECOMBINATION; SOMATIC HYPERMUTATION; ADAPTIVE IMMUNITY; INNATE; RESPONSES; IGM; LIGATION;
D O I
10.1038/cmi.2012.61
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Expression of Toll-like receptors (TLRs) in B cells provides a cell-intrinsic mechanism for innate signals regulating adaptive immune responses. In combination with other signaling pathways in B cells, including through the B-cell receptor (BCR), TLR signaling plays multiple roles in B-cell differentiation and activation. The outcome of TLR signaling in B cells is largely context-dependent, which partly explains discrepancies among in vitro and in vivo studies, or studies using different immunogens. We focus on recent findings on how B-cell-intrinsic TLR signaling regulates antibody responses, including germinal center formation and autoantibody production in autoimmune disease models. In addition, TLR signaling also acts on the precursors of B cells, which could influence the immune response of animals by shaping the composition of the immune system. With TLR signaling modulating immune responses at these different levels, much more needs to be understood before we can depict the complete functions of innate signaling in host defense. Cellular & Molecular Immunology (2013) 10, 103-106; doi: 10.1038/cmi.2012.61; published online 17 December 2012
引用
收藏
页码:103 / 106
页数:4
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