Mitochondrial response to fever boosts TH1-driven inflammatory responses-Immunometabolism-CSCIED科技核心评价数据库-手机版

Mitochondrial response to fever boosts TH1-driven inflammatory responses

Mitochondrial response to fever boosts TH1-driven inflammatory responses

ES评分 0 浏览量：1177 下载量：0

DOI	10.1097/IN9.0000000000000058
刊名	Immunometabolism IJ
年，卷(期)	2025, 7(2)
作者	Dunphy, Gillian; Sancho, David,
作者单位	[Dunphy, Gillian; Sancho, David] Ctr Nacl Invest Cardiovasc CNIC, Immunobiol Lab, Madrid, Spain
摘要	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 degrees C) on T cell function. They describe increased T(H)1 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.
Abstract	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 degrees C) on T cell function. They describe increased T(H)1 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.
关键词	mitochondria; fever; inflammation; T(H)1 immunity
KeyWord	mitochondria; fever; inflammation; T(H)1 immunity
基金项目
页码	1-3

参考文献
相关文献

[1]. Saravia J, Chapman NM, Chi H. Helper T cell differentiation. Cell Mol Immunol. 2019;16:634-43.

[2]. Kurmi K, Liang D, van de Ven R, et al. Metabolic modulation of mitochondrial mass during CD4+ T cell activation. Cell Chem Biol. 2023;30:1064-75.e8.

[3]. Baixauli F, Piletic K, Puleston DJ, et al. An LKB1-mitochondria axis controls TH17 effector function. Nature. 2022;610:555-61.

[4]. Raynor JL, Chi H. Nutrients: signal 4 in T cell immunity. J Exp Med. 2024;221:e20221839.

[5]. Wu H, Estrella V, Beatty M, et al. T-cells produce acidic niches in lymph nodes to suppress their own effector functions. Nat Commun. 2020;11(1):4113.

[6]. Evans SS, Repasky EA, Fisher DT. Fever and the thermal regulation of immunity: the immune system feels the heat. Nat Rev Immunol. 2015;15:335-49.

[7]. Lin C, Zhang Y, Zhang K, et al. Fever promotes T lymphocyte trafficking via a thermal sensory pathway involving heat shock protein 90 and α4 integrins. Immunity. 2019;50:137-51.e6.

[8]. Mace TA, Zhong L, Kilpatrick C, et al. Differentiation of CD8+ T cells into effector cells is enhanced by physiological range hyperthermia. J Leukoc Biol. 2011;90:951-62.

[9]. O’Sullivan D, Stanczak MA, Villa M, et al. Fever supports CD8 , effector T cell responses by promoting mitochondrial translation. Proc Natl Acad Sci U S A. 2021;118:e2023752118.

[10]. Wang X, Ni L, Wan S, et al. Febrile temperature critically controls the differentiation and pathogenicity of T Helper 17 cells. Immunity. 2020;52:328-41.e5.

[11]. Umar D, Das A, Gupta S, et al. Febrile temperature change modulates CD4 T cell differentiation via a TRPV channel-regulated Notch-dependent pathway. Proc Natl Acad Sci USA. 2020;117:22357-66.

[12]. Heintzman DR, Sinard RC, Fisher EL, et al. Subset-specific mitochondrial stress and DNA damage shape T cell responses to fever and inflammation. Sci Immunol. 2024;9:eadp3475.

[13]. Gehrke N, Mertens C, Zillinger T, et al. Oxidative damage of DNA confers resistance to cytosolic nuclease TREX1 degradation and potentiates STING-dependent immune sensing. Immunity. 2013;39:482-95.

[14]. Chrétien D, Bénit P, Ha HH, et al. Mitochondria are physiologically maintained at close to 50 °C. PLoS Biol. 2018;16:e2003992.

[15]. Jarzab A, Kurzawa N, Hopf T, et al. Meltome atlas—thermal proteome stability across the tree of life. Nat Methods. 2020;17:495-503.

[16]. Turner L, Van Le TN, Cross E, et al. Single-cell NAD(H) levels predict clonal lymphocyte expansion dynamics. Sci Immunol. 2024;9:eadj7238.

[17]. Cameron AM, Castoldi A, Sanin DE, et al. Inflammatory macrophage dependence on NAD + salvage is a consequence of reactive oxygen species–mediated DNA damage. Nat Immunol. 2019;20(4):420-32.

[18]. Chi H. Regulation and function of mTOR signalling in T cell fate decisions. Nat Rev Immunol. 2012;12:325-38.

[19]. Delgoffe GM, Kole TP, Zheng Y, et al. The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment. Immunity. 2009;30:832-44.

[20]. Michalek RD, Gerriets VA, Jacobs SR, et al. Cutting edge: distinct glycolytic and lipid oxidative metabolic programs are essential for effector and regulatory CD4+ T cell subsets. J Immunol. 2011;186:3299-303.

[21]. Bailis W, Shyer JA, Zhao J, et al. Distinct modes of mitochondrial metabolism uncouple T cell differentiation and function. Nature. 2019;571(7765):403-7.

[22]. Johnnidis JB, Muroyama Y, Ngiow SF, et al. Inhibitory signaling sustains a distinct early memory CD8 , T cell precursor that is resistant to DNA damage. Sci Immunol. 2021;6:eabe3702.

[23]. Goodnow CC. Multistep pathogenesis of autoimmune disease. Cell. 2007;130:25-35.

[24]. Savola P, Kelkka T, Rajala HL, et al. Somatic mutations in clonally expanded cytotoxic T lymphocytes in patients with newly diagnosed rheumatoid arthritis. Nat Commun. 2017;8:15869.,

引用本文

Dunphy, Gillian; Sancho, David. Mitochondrial response to fever boosts TH1-driven inflammatory responses [J]. Immunometabolism. 2025; 7; (2). 1 - 3.

文献评论

相关学者

相关机构