High TLR7 Expression Drives the Expansion of CD19⁺CD24^hiCD38^hi Transitional B Cells and Autoantibody Production in SLE Patients.

ABSTRACT: Signaling through Toll-like receptor 7 (TLR7) drives the production of type I IFN and promotes the activation of autoreactive B cells and is implicated in the pathogenesis of systemic lupus erythematosus (SLE). While TLR7 has been extensively studied in murine lupus, much less is known about its role in the pathogenesis of human SLE. Genetic studies support a link between the TLR7 rs3853839 C/G polymorphism, which affects TLR7 mRNA turnover, and SLE susceptibility; however, the effects of this polymorphism on B cells have not been studied. Here we determined how changes in TLR7 expression affect peripheral B cells and auto-Ab production in SLE patients. High TLR7 expression in SLE patients driven by TLR7 rs3853839 C/G polymorphism was associated with more

SUBMITTER: Wang T 

PROVIDER: S-EPMC6559307 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature