Abstract
Follicular regulatory T (Tfr) cells are the regulatory T cell subset mainly localized in the germinal center (GC), acting as modulators of GC responses. They can disrupt Tfh cell- and B cell-linked recognition, induce Tfh apoptosis, and suppress B cell function. Evidences show that dysregulated Tfr cells are associated with the disease activity index and serum autoantibody levels, influencing the development of systemic lupus erythematosus (SLE). This review focuses on the interaction among Tfr, Tfh, and B cells, summarizes the characterization and function of Tfr cells, concludes the imbalance of CD4+T subsets in SLE, and presents potential therapies for SLE. In general, we discuss the roles of Tfr cells in the progress of SLE and provide potential treatments.
Highlights
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by red speckles on the skin and multiple organ damage
Current studies have revealed that imbalance of T helper (Th) cell subsets and regulatory T (Treg) cell subsets may contribute to the pathogenesis of SLE [1]
In the progress of studying the relationship between Tfr cells and disease activity, it was found that there was a positive correlation between CD4+CXCR5+ cells and SLE disease activity index (SLEDAI) scores, and the Tfr/Tfh ratios were positively correlated with SLEDAI scores
Summary
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by red speckles on the skin and multiple organ damage. Current studies have revealed that imbalance of T helper (Th) cell subsets and regulatory T (Treg) cell subsets may contribute to the pathogenesis of SLE [1]. Previous studies showed that there were increased peripheral follicular helper T (Tfh) cells in autoimmune and inflammation diseases [2, 3]. Follicular regulatory T (Tfr) cells are the regulatory T cell subset mainly localized in germinal centers (GCs). It is suggested that Tfr cells can mediate Tfh and B cell reactions for proper GC responses [4]. We discuss the features and roles of Tfr cells in SLE
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