Systemic lupus erythematosus (SLE) is a complex autoimmune disease with multifaceted pathogenetic processes, including abnormalities of T‐cell subset distribution and function. Accumulation of senescent CD4 + T cells has been found to contribute to the development of the disease. In this issue, Jiang et al. provide compelling evidence that links an expanded pool of CD4 + CD57 + senescent T cells in patients with SLE to disease activity favored by interleukin‐15. Importantly, treatment of lupus‐prone mice with a senolytic drug resulted in decreased autoimmune pathology. The findings of this study suggest possible novel therapeutics to treat patients with SLE.
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Pan et al. (2024) studied this question.
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