Purpose of review: Systemic lupus erythematosus is a complex disease with broad spectrum of clinical manifestations. In addition to abnormal B cell responsive leading to autoantibody production, various T cells also play different roles in promoting systemic autoimmunity and end organ damage. We aim to provide a review on recent developments in how abnormalities in different T cells subsets contribute to systemic lupus erythematosus pathogenesis and how they inform the consideration of new promising therapeutics.
Recent findings: Distinct subsets of T cells known as T follicular helper cells enable the production of pathogenic autoantibodies. Detailed understanding of the B cell helping T cell subsets should improve the performance of clinical trials targeting the cognate T:B cell interaction. CD8+ T cells play a role in peripheral tolerance and reversal of its exhausted phenotype could potentially alleviate both systemic autoimmunity and the risk of infection. Research on the abnormal lupus T cell signaling also leads to putative therapeutic targets able to restore interleukin-2 production and suppress the production of the pathogenic IL-17 cytokine. Recently, several studies have focused on dissecting T cell populations located in the damaged organs, aiming to target the pathogenic processes specific to each organ. Numerous T cell subsets play distinct roles in SLE pathogenesis and recent research in understanding abnormal signaling pathways, cellular metabolism, and environmental cues pave the way for the development of novel therapeutics.
Keywords: Lupus; SLE; T cells.