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Here, we show that disruption of Golgi architecture under TME stress, identified by the decreased expression of GM130, was reverted upon treatment with hydrogen sulfide (H\n                    <jats:sub>2<\/jats:sub>\n                    S) donor GYY4137 or overexpressing cystathionine \u03b2-synthase (CBS), an enzyme involved in the biosynthesis of endogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S, which also promoted stemness, antioxidant capacity, and increased protein translation, mediated in part by endoplasmic reticulum\u2013Golgi shuttling of Peroxiredoxin-4. In in vivo models of melanoma and lymphoma, antitumor T cells conditioned ex vivo with exogenous H\n                    <jats:sub>2<\/jats:sub>\n                    S or overexpressing CBS demonstrated superior tumor control upon adoptive transfer. Further, T cells with high Golgi content exhibited unique metabolic and glycation signatures with enhanced antitumor capacity. These data suggest that strategies to mitigate Golgi network stress or using Golgi\n                    <jats:sup>hi<\/jats:sup>\n                    tumor-reactive T cells can improve tumor control upon adoptive transfer.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.adp1152","type":"journal-article","created":{"date-parts":[[2024,11,15]],"date-time":"2024-11-15T13:58:57Z","timestamp":1731679137000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":24,"title":["H\n                    <sub>2<\/sub>\n                    S-Prdx4 axis mitigates Golgi stress to bolster tumor-reactive T cell immunotherapeutic response"],"prefix":"10.1126","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9080-5130","authenticated-orcid":true,"given":"Nathaniel","family":"Oberholtzer","sequence":"first","affiliation":[{"name":"Department of Surgery, Medical University of South Carolina, Charleston, SC 29425, 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