{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Heintzman DR"],"funding":["NEI NIH HHS","NIDDK NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","NCI NIH HHS","NIAMS NIH HHS"],"pagination":["eadp3475"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11607909"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(99)"],"pubmed_abstract":["Heat is a cardinal feature of inflammation, yet its impacts on immune cells remain uncertain. We show that moderate-grade fever temperatures (39°C) increased murine CD4 T cell metabolism, proliferation, and inflammatory effector activity while decreasing regulatory T cell suppressive capacity. However, heat-exposed T helper 1 (T<sub>H</sub>1) cells selectively developed mitochondrial stress and DNA damage that activated Trp53 and stimulator of interferon genes pathways. Although many T<sub>H</sub>1 cells subjected to such temperatures died, surviving T<sub>H</sub>1 cells exhibited increased mitochondrial mass and enhanced activity. Electron transport chain complex 1 (ETC1) was rapidly impaired under fever-range temperatures, a phenomenon that was specifically detrimental to T<sub>H</sub>1 "],"journal":["Science immunology"],"pubmed_title":["Subset-specific mitochondrial stress and DNA damage shape T cell responses to fever and inflammation."],"pmcid":["PMC11607909"],"funding_grant_id":["R01 AI153167","P30 DK058404","R01 HL136664","R01 HL118979","R01 CA217987","P30 EY008126","R01 DK105550","T32 DK101003","T32 AI112541","P30 DK020593","P30 CA068485","K00 CA253718","U2C DK059637","T32 AR059039","R01 CA245134","U01 AI176244"],"pubmed_authors":["Khan W","Chi C","Bass L","Toudji YT","Mason FM","Rathmell JC","Ye X","Newcomb DC","Wilson JT","Elasy JH","Beier KL","Deng W","Heintzman DR","Rodriguez-Garcia GJ","Patterson AR","Hong HS","Sinard RC","Steiner KK","Olson LM","Rathmell WK","Chowdhury NU","Sugiura A","Arner EN","Voss K","Jones AL","Krystoviak ES","Fisher EL","Bick AG","Lyssiotis CA"],"additional_accession":[]},"is_claimable":false,"name":"Subset-specific mitochondrial stress and DNA damage shape T cell responses to fever and inflammation.","description":"Heat is a cardinal feature of inflammation, yet its impacts on immune cells remain uncertain. We show that moderate-grade fever temperatures (39°C) increased murine CD4 T cell metabolism, proliferation, and inflammatory effector activity while decreasing regulatory T cell suppressive capacity. However, heat-exposed T helper 1 (T<sub>H</sub>1) cells selectively developed mitochondrial stress and DNA damage that activated Trp53 and stimulator of interferon genes pathways. Although many T<sub>H</sub>1 cells subjected to such temperatures died, surviving T<sub>H</sub>1 cells exhibited increased mitochondrial mass and enhanced activity. Electron transport chain complex 1 (ETC1) was rapidly impaired under fever-range temperatures, a phenomenon that was specifically detrimental to T<sub>H</sub>1 ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-06-03T11:33:24.09Z","creation":"2026-04-27T03:10:34.533Z"},"accession":"S-EPMC11607909","cross_references":{"pubmed":["39303018"],"doi":["10.1126/sciimmunol.adp3475"]}}