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Merck

Arthritis flares mediated by tissue-resident memory T cells in the joint.

Cell reports (2021-10-28)
Margaret H Chang, Anaïs Levescot, Nathan Nelson-Maney, Rachel B Blaustein, Kellen D Winden, Allyn Morris, Alexandra Wactor, Spoorthi Balu, Ricardo Grieshaber-Bouyer, Kevin Wei, Lauren A Henderson, Yoichiro Iwakura, Rachael A Clark, Deepak A Rao, Robert C Fuhlbrigge, Peter A Nigrovic
RESUMEN

Rheumatoid arthritis is a systemic autoimmune disease, but disease flares typically affect only a subset of joints, distributed in a distinctive pattern for each patient. Pursuing this intriguing pattern, we show that arthritis recurrence is mediated by long-lived synovial resident memory T cells (TRM). In three murine models, CD8+ cells bearing TRM markers remain in previously inflamed joints during remission. These cells are bona fide TRM, exhibiting a failure to migrate between joints, preferential uptake of fatty acids, and long-term residency. Disease flares result from TRM activation by antigen, leading to CCL5-mediated recruitment of circulating effector cells. Correspondingly, TRM depletion ameliorates recurrence in a site-specific manner. Human rheumatoid arthritis joint tissues contain a comparable CD8+-predominant TRM population, which is most evident in late-stage leukocyte-poor synovium, exhibiting limited T cell receptor diversity and a pro-inflammatory transcriptomic signature. Together, these findings establish synovial TRM as a targetable mediator of disease chronicity in autoimmune arthritis.

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