Systemic lupus erythematosus (SLE) is an autoimmune disease characteristic of the immune complex-induced chronic inflammatory damages. The high-affinity pathogenic autoantibodies, which primarily originate from the self-reactive B cells underwent somatic hypermutation and class switch, principally but not exclusively, in germinal centers, contribute substantially to the inflammatory damages of multiple organs in SLE. Follicular helper T (T(FH)) cells constitute a distinct CD4+ T helper population beyond the Th1/Th2 paradigm. T(FH) cells can be critical for providing help to B cells allowing the formation of germinal center and the subsequent long-lived plasma cells differentiation. There is a growing body of evidence by far pointing toward the crucial roles of T(FH) cells in the overproduction of pathogenic autoantibodies and tissue damages in SLE. This article concerns the expansion and pathogenic mechanisms of T(FH) cells in SLE, and in particular, potential therapeutic implications for targeting T(FH) cells in this immunopathologically complicated disease.
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