{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,7]],"date-time":"2026-09-07T13:09:33Z","timestamp":1788786573920,"version":"build-2803163510"},"reference-count":79,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["CA257954"],"award-info":[{"award-number":["CA257954"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>T cell exhaustion remains a significant barrier to effective adoptive cell therapy in solid tumors. Here, we demonstrate that in vitro treatment with the PI3K\u03b4 inhibitor CAL-101 generates T cells with enhanced stemness and metabolic fitness. These cells show increased mitochondrial dependence and spare respiratory capacity while maintaining normal basal metabolism. Under chronic antigen stimulation, CAL-101\u2013treated T cells, including human T cells, resist terminal exhaustion and maintain stem-like properties. Using single-cell RNA sequencing and spatial transcriptomics of B16 melanoma tumors, we found that CAL-101\u2013treated T cells preferentially differentiate into progenitor exhausted T cells within the tumor microenvironment. These cells demonstrate enhanced tumor infiltration and upregulate the Cxcl10\/Cxcr3 signaling axis. The tumor microenvironment of tumors containing CAL-101\u2013treated T cells show reduced glycolysis, oxidative phosphorylation, and proliferation, while exhibiting increased proinflammatory signaling and decreased presence of immunosuppressive tumor-associated macrophages. Single-cell analysis reveals that the CAL-10\u2013treated T cells concurrently increase oxidative phosphorylation, proliferation, and immune signaling pathways. Mechanistically, CAL-101\u2013treated T cells maintain high expression of stemness-associated genes (Tcf7, Slamf6) while resisting expression of genes associated with terminal exhaustion (Tim3, Mt1\/2). These findings reveal the mechanisms behind how PI3K\u03b4 inhibition generates T cells capable of establishing and maintaining an antitumor immune response, suggesting a promising strategy for improving adoptive cell therapy outcomes in solid tumors.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag108","type":"journal-article","created":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T23:40:16Z","timestamp":1780098016000},"source":"Crossref","is-referenced-by-count":0,"title":["PI3K\u03b4 inhibition alters CD8 T cell differentiation and reprograms the tumor microenvironment following adoptive immunotherapy"],"prefix":"10.1093","volume":"215","author":[{"given":"Alexandrea","family":"Turnquist","sequence":"first","affiliation":[{"name":"Geisel School of Medicine at Dartmouth College Department of Microbiology and Immunology, , Lebanon, NH,","place":["United 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