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Fever supports CD8+ effector T cell responses by promoting mitochondrial translation

ABSTRACT: Fever supports CD8+ effector T cell responses by promoting mitochondrial translation

PROVIDER: PRJNA718850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14119167_1.fastq.gz	Fastqsanger.gz
	SRR14119167_2.fastq.gz	Fastqsanger.gz
	SRR14119168_1.fastq.gz	Fastqsanger.gz
	SRR14119168_2.fastq.gz	Fastqsanger.gz
	SRR14119169_1.fastq.gz	Fastqsanger.gz

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Fever supports CD8+ effector T cell responses by promoting mitochondrial translation

Project description:Fever can provide a survival advantage during infection. Metabolic processes are sensitive to environmental conditions, but the effect of fever on T cell metabolism is not well characterized. We show that in activated CD8+ T cells, exposure to febrile temperature (39°C) augmented metabolic activity and T cell effector functions, despite having a limited effect on proliferation or activation marker expression. Transcriptional profiling revealed an upregulation of mitochondrial pathways, which was consistent with increased mitochondrial metabolism and mass observed in T cells exposed to 39°C. Through in vitro and in vivo models we determined that mitochondrial translation is integral to the enhanced metabolic activity and function of CD8+ T cells exposed to febrile temperature. Transiently exposing donor lymphocytes to 39°C prior to infusion in a myeloid leukemia (ML) mouse model conferred enhanced therapeutic efficacy, raising the possibility that exposure of T cells to febrile temperatures could have clinical potential.

2021-07-02 | GSE171245 | GEO

Fever supports CD8+ effector T cell responses by promoting mitochondrial translation.

Project description:Fever can provide a survival advantage during infection. Metabolic processes are sensitive to environmental conditions, but the effect of fever on T cell metabolism is not well characterized. We show that in activated CD8+ T cells, exposure to febrile temperature (39 °C) augmented metabolic activity and T cell effector functions, despite having a limited effect on proliferation or activation marker expression. Transcriptional profiling revealed an up-regulation of mitochondrial pathways, which was consistent with increased mass and metabolism observed in T cells exposed to 39 °C. Through in vitro and in vivo models, we determined that mitochondrial translation is integral to the enhanced metabolic activity and function of CD8+ T cells exposed to febrile temperature. Transiently exposing donor lymphocytes to 39 °C prior to infusion in a myeloid leukemia mouse model conferred enhanced therapeutic efficacy, raising the possibility that exposure of T cells to febrile temperatures could have clinical potential.

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Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

Project description:Cytosolic N6AMT1-dependent translation supports mitochondrial RNA processing [Ribo-seq]

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Cold-blooded vertebrate utilizes behavioral fever to alleviate T-cell apoptosis and optimize antimicrobial immunity

Project description:Fever confers significant survival benefits on endotherms by optimizing both innate and adaptive immunity. Ectotherms achieve thermoregulation using behavioral strategies, but existing evidence supports its enhancement effect on innate immunity only. Therefore, it remains unknown whether the coordination between fever and adaptive immunity was independently acquired by endotherms or instead represents a gradually evolved function common to vertebrates. In the present study, we reported that Nile tilapia developed behavioral fever to enhance the immune response against Edwardsiella piscicida infection. Behavioral fever lasted five days, and the immune potential was optimized at 4–6 days post infection, indicating a potential correlation between fever events and T-cell immunity. Further investigation suggested that fever did not affect T-cell activation or proliferation but improved the ability of T cells to produce IFN- and Granzyme B and enhanced cytotoxicity, thereby eliminating the infection more effectively. Notably, we identified a previously unknown advantage conferred by fever during infection: alleviation of T-cell apoptosis to maintain a considerable T-cell pool. Mechanistically, fever induced the expression of HSP70, which in turn entered the nucleus and bound to and promoted the phosphorylation of ERK1/2, thereby inhibiting the cleavage of caspase-8/caspase-3 and preventing T-cell apoptosis. Our findings elucidate the detailed mechanism by which behavioral fever optimizes T-cell immunity in a cold-blooded vertebrate and propose that integrating fever with adaptive immunity to gain survival advantages is an ancient strategy acquired before the emergence of tetrapod.

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