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.
Keywords: B-1 B cells; Unc-93 Homolog B1 (C. elegans) (Unc93b1); anti-nuclear autoantibody (ANA); germinal center B cells (GC B cells); marginal zone B cells (MZ B cells); memory B cells; myeloid differentiation primary response gene 88 (MyD88); systemic lupus erythematosus (SLE); toll-like receptor (TLR); transitional B cells.