Roles of B Cell-Intrinsic TLR Signals in Systemic Lupus Erythematosus

被引：39

作者：

Ma, Kongyang ^{[1
,2
]}

Li, Jingyi ^{[3
]}

Fang, Yongfei ^{[3
]}

Lu, Liwei ^{[1
,2
]}

机构：

[1] Univ Hong Kong, Dept Pathol, Hong Kong, Hong Kong, Peoples R China

[2] Univ Hong Kong, Ctr Infect & Immunol, Shenzhen Inst Res & Innovat, Hong Kong, Hong Kong, Peoples R China

[3] Third Mil Med Univ, Southwest Hosp, Dept Rheumatol, Chongqing 400038, Peoples R China

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2015年 / 16卷 / 06期

基金：

中国国家自然科学基金;

关键词：

TOLL-LIKE RECEPTORS; MARGINAL ZONE; AUTOANTIBODY PRODUCTION; INCREASED FREQUENCY; AUTOIMMUNE-DISEASE; DENDRITIC CELLS; STRENGTH DETERMINES; NEGATIVE REGULATION; ENDOGENOUS LIGANDS; GERMINAL-CENTERS;

D O I：

10.3390/ijms160613084

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Toll-like receptors (TLRs) are a large family of pattern recognition receptors. TLR signals are involved in the pathogenesis of systemic lupus erythematosus. Mouse and human B cells constitutively express most TLRs. Many B cell subpopulations are highly responsive to certain TLR ligation, including B-1 B cells, transitional B cells, marginal zone B cells, germinal center B cell and memory B cells. The B cell-intrinsic TLR signals play critical roles during lupus process. In this review, roles of B cell-intrinsic TLR2, 4, 7, 8 and 9 signals are discussed during lupus pathogenesis in both mouse model and patients. Moreover, mechanisms underlying TLR ligation-triggered B cell activation and signaling pathways are highlighted.

引用

页码：13084 / 13105

页数：22

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