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It is a triterpenoid compound that activates nuclear factor erythroid 2-related factor 2 (NRF2), a key regulator of cellular redox balance. In this study, we explored the impact of RTA-408 on T cells and evaluated its therapeutic potential in inflammatory bowel disease (IBD). In vitro activation of murine and human T cells in the presence of RTA-408 resulted in suppressed proliferation, reduced expression of IFN-\u03b3, cytotoxic granules and IL-17, but enhanced frequency of Foxp3+ Treg cells. Treatment of Nrf2-deficient T cells with RTA-408 revealed that while the reduction in CD69 expression, IL-2, and IFN-\u03b3 levels is NRF2-dependent, the suppression of T cell proliferation and granzyme B\/perforin expression occurs independently of NRF2. In vivo administration of RTA-408 alleviated the disease severity in DSS-induced colitis mice by decreasing colonic T cell counts and their inflammatory cytokine production. Additionally, ex vivo treatment of T cells from IBD patients with RTA-408 reduced their expansion and IL-17 expression. Transcriptomic and metabolic analyses revealed that RTA-408 reduces glycolysis and mitochondrial respiration in T cells and reprograms their metabolism towards pentose phosphate pathway and glutaminolysis. Our findings highlight the potential of RTA-408 as a modulator of T cell homeostasis, metabolism, and inflammation, supporting its repurposing for inflammatory diseases like IBD.<\/jats:p>","DOI":"10.1093\/jimmun\/vkaf117","type":"journal-article","created":{"date-parts":[[2025,6,26]],"date-time":"2025-06-26T14:10:41Z","timestamp":1750947041000},"page":"1951-1968","source":"Crossref","is-referenced-by-count":8,"title":["Therapeutic potential of NRF2 activating drug RTA-408 in suppressing T cell effector responses and inflammatory bowel disease"],"prefix":"10.1093","volume":"214","author":[{"given":"Debolina","family":"Dasgupta","sequence":"first","affiliation":[{"name":"Department of Cancer Biology, University of Kansas, Medical Center , Kansas City, KS,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aprajita","family":"Tripathi","sequence":"additional","affiliation":[{"name":"Department of Cancer Biology, University of Kansas, Medical Center 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