2026-05-17T00:20:35Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/268272025-12-18T13:01:56Zcom_20.500.12105_19586com_20.500.12105_2202col_20.500.12105_19587
Repisalud
author
Dunphy, Gillian
author
Sancho, David
funder
Unión Europea. Comisión Europea. H2020
funder
Unión Europea. Comisión Europea. European Research Council (ERC)
funder
Ministerio de Ciencia, Innovación y Universidades (España)
funder
Agencia Estatal de Investigación (España)
funder
Unión Europea. Comisión Europea. NextGenerationEU
funder
Comunidad de Madrid (España)
funder
Asociación Española Contra el Cáncer
funder
Fundación La Caixa
2025-07-16T11:00:59Z
2025-07-16T11:00:59Z
2025-04
Immunometabolism (Cobham). 2025 Mar 13;7(2):e00058.
IMMUNOMETABOLISM
40092481
https://hdl.handle.net/20.500.12105/26827
Increased body temperature, both locally and systemically, is a key feature of the inflammatory response. Heat is associated with increased blood flow to affected areas and increased immune infiltrate, yet increased temperature has also been described to have direct effects on immune cell function. In a recent study, Heintzman, et al investigated the effect of febrile temperature (39 °C) on T cell function. They describe increased T1 function and fitness accompanied by a decrease in regulatory T cell suppressive function. These findings add another important consequence to our understanding of fever responses.
eng
TH1 immunity
fever
inflammation
mitochondria
Mitochondrial response to fever boosts T1-driven inflammatory responses.
research article
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URL
https://repisalud.isciii.es/bitstreams/44d986ca-a53b-44f5-93bf-417028f9e409/download
File
MD5
a1afaaf13b72a17cd8f8ecb9fad833b2
389903
application/pdf
Mitochondrial response_Immunometabolism_2025.pdf