{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["27(5)"],"submitter":["Bopp L"],"funding":["Deutsche Forschungsgemeinschaft","Michael Smith Foundation for Health Research"],"pubmed_abstract":["T cells protect tissues from cancer. Although investigations in mice showed that amino acids (AA) critically regulate T cell immunity, this remains poorly understood in humans. Here, we describe the AA composition of interstitial fluids in keratinocyte-derived skin cancers (KDSCs) and study the effect of AA on T cells using models of primary human cells and tissues. Gln contributed to ∼15% of interstitial AAs and promoted interferon gamma (IFN-γ), but not granzyme B (GzB) expression, in CD8<sup>+</sup> T cells. Furthermore, the Toll-like receptor 7 agonist imiquimod (IMQ), a common treatment for KDSCs, down-regulated the metabolic gatekeepers <i>c-MYC</i> and mTORC1, as well as the AA transporter ASCT2 and intracellular Gln, Asn, Ala, and Asp in T cells. Reduced proliferation and IFN-γ exp"],"journal":["iScience"],"pagination":["109767"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11088342"],"repository":["biostudies-literature"],"pubmed_title":["Glutamine promotes human CD8<sup>+</sup> T cells and counteracts imiquimod-induced T cell hyporesponsiveness."],"pmcid":["PMC11088342"],"pubmed_authors":["Brodesser S","Martinez ML","Lackmann JW","Bopp L","Lukas D","Arana MH","Oh JH","Brachvogel B","Seitz R","Neumayer D","Klapproth H","Mueller S","von Stebut E","Klein Geltink RI","Schumacher C","Fabri M"],"additional_accession":[]},"is_claimable":false,"name":"Glutamine promotes human CD8<sup>+</sup> T cells and counteracts imiquimod-induced T cell hyporesponsiveness.","description":"T cells protect tissues from cancer. Although investigations in mice showed that amino acids (AA) critically regulate T cell immunity, this remains poorly understood in humans. Here, we describe the AA composition of interstitial fluids in keratinocyte-derived skin cancers (KDSCs) and study the effect of AA on T cells using models of primary human cells and tissues. Gln contributed to ∼15% of interstitial AAs and promoted interferon gamma (IFN-γ), but not granzyme B (GzB) expression, in CD8<sup>+</sup> T cells. Furthermore, the Toll-like receptor 7 agonist imiquimod (IMQ), a common treatment for KDSCs, down-regulated the metabolic gatekeepers <i>c-MYC</i> and mTORC1, as well as the AA transporter ASCT2 and intracellular Gln, Asn, Ala, and Asp in T cells. Reduced proliferation and IFN-γ exp","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 May","modification":"2026-06-03T04:21:43.441Z","creation":"2026-04-24T03:10:00.176Z"},"accession":"S-EPMC11088342","cross_references":{"pubmed":["38736545"],"doi":["10.1016/j.isci.2024.109767"]}}