Abstract
Abstract Autoantibodies against nuclear antigens secreted by autoreactive B cells are a hallmark of systemic autoimmunity. Failure to eliminate autoreactive B cells in the germinal center reaction has been reported in lupus disease. We have recently shown that TLR7 duplication in Yaa mice accelerates the onset of lupus disease. To better understand TLR7 roles in the pathogenesis of lupus disease, we created transgenic TLR7 (B6.Tg. TLR7) mice. We found an increase of spontaneous germinal center formation in both B6.Tg. TLR7 mice and B6. Yaa which is TLR7 dependent. We have carried out microarray analysis of gene expression profiles of follicular B cells (CD9-CD43-) from B6.Tg. TLR7 compared to B6. The upregulated genes in B6.Tg. TLR7 consist of interferon inducible genes, cell cycle regulators, MHC, and immunoglobulin genes. We have confirmed increased protein expression of phosphorylated stat1 (Ser727) by western blot and of H2-Ab1 by flow cytometry in B6.Tg. TLR7. These results suggest the possibility of increased antigen presentation by TLR7-overexpressing B cells in the high interferon environment.
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