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.

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.