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Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE247863 | GEO | 2023/12/23

REPOSITORIES: GEO

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Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [RNA-seq]

Project description:The tissue accumulation of T cells expressing the transcription factor Eomesodermin (Eomes) has been reported in several chronic inflammatory diseases, including multiple sclerosis. However, the mechanisms whereby Eomes controls this accumulation and strengthens inflammation remains ill-defined. Here, we show that Eomes deletion in antigen-specific CD4+ T cells is sufficient to protect against central nervous system (CNS) inflammation. We demonstrate that Eomes is dispensable for the initial priming of CD4+ T cells but is required for long-term maintenance of CNS-infiltrating CD4+ T cells. Our transcriptomic studies reveal that the impact Eomes on effector CD4+ T cell longevity is associated with sustained expression of multiple genes involved in mitochondrial organization and function. Accordingly, epigenetic studies demonstrate that Eomes supports mitochondrial function by direct binding to either metabolism-associated genes or mitochondrial transcriptional modulators. Besides, the significance of these findings was confirmed in both healthy donors and multiple sclerosis patients. CD4+ T cells expressing Eomes exhibit enhanced mitochondrial functions, which resulted in their increased capacity to survive upon prolonged in vitro stimulation. Together, our data reveal a new mechanism by which Eomes promotes severity and chronicity of inflammation via the enhancement of CD4+ T cell mitochondrial functions and resistance to stress-induced cell death.

2023-12-23 | GSE247862 | GEO

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [CUT&RUN]

2023-12-23 | GSE247861 | GEO

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [ATAC-seq]

2023-12-23 | GSE247860 | GEO

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation

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Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [CUT&RUN]

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [CUT&RUN]

| PRJNA1040833 | ENA

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [ATAC-seq]

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [ATAC-seq]

| PRJNA1040832 | ENA

Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [RNA-seq]

Project description:Eomes regulates mitochondrial function and promotes survival of pathogenic CD4+ T cells during chronic inflammation [RNA-seq]

| PRJNA1040834 | ENA

Calcium Signaling Controls Pathogenic Th17 Cell-Mediated Inflammation by Regulating Mitochondrial Function.

Project description:Pathogenic Th17 cells play important roles in many autoimmune and inflammatory diseases. Their function depends on T cell receptor (TCR) signaling and cytokines that activate signal transducer and activator of transcription 3 (STAT3). TCR engagement activates stromal interaction molecule 1 (STIM1) and calcium (Ca2+) influx through Ca2+-release-activated Ca2+ (CRAC) channels. Here, we show that abolishing STIM1 and Ca2+ influx in T cells expressing a hyperactive form of STAT3 (STAT3C) attenuates pathogenic Th17 cell function and inflammation associated with STAT3C expression. Deletion of STIM1 in pathogenic Th17 cells reduces the expression of genes required for mitochondrial function and oxidative phosphorylation (OXPHOS) but enhances reactive oxygen species (ROS) production. STIM1 deletion or inhibition of OXPHOS is associated with a non-pathogenic Th17 gene expression signature and impaired pathogenic Th17 cell function. Our findings establish Ca2+ influx as a critical regulator of mitochondrial function and oxidative stress in pathogenic Th17 cell-mediated multiorgan inflammation.

| S-EPMC6506368 | biostudies-literature

TGFbRII-Eomes in CD4 T cells during chronic viral infection

Project description:Transcriptome analysis of CD4+ PD1+ T cells during LCMV CL13 infection Gene expression in WT and ERt2-cre;TGFbRII flox virus specific CD4 T cells Mixed chimeras of WT:ERt2cre+TGFbRII flox/flox were infected 9 days with LCMV and splenic CD4+ PD1+CD49d+ Cd8a- T cells sorted from each compartment by congenic marker

2016-06-30 | E-GEOD-83921 | biostudies-arrayexpress

Lymphatic endothelial S1P promotes mitochondrial function and survival in naive T cells.

Project description:Effective adaptive immune responses require a large repertoire of naive T cells that migrate throughout the body, rapidly identifying almost any foreign peptide. Because the production of T cells declines with age, naive T cells must be long-lived. However, it remains unclear how naive T cells survive for years while constantly travelling. The chemoattractant sphingosine 1-phosphate (S1P) guides T cell circulation among secondary lymphoid organs, including spleen, lymph nodes and Peyer's patches, where T cells search for antigens. The concentration of S1P is higher in circulatory fluids than in lymphoid organs, and the S1P1 receptor (S1P1R) directs the exit of T cells from the spleen into blood, and from lymph nodes and Peyer's patches into lymph. Here we show that S1P is essential not only for the circulation of naive T cells, but also for their survival. Using transgenic mouse models, we demonstrate that lymphatic endothelial cells support the survival of T cells by secreting S1P via the transporter SPNS2, that this S1P signals through S1P1R on T cells, and that the requirement for S1P1R is independent of the established role of the receptor in guiding exit from lymph nodes. S1P signalling maintains the mitochondrial content of naive T cells, providing cells with the energy to continue their constant migration. The S1P signalling pathway is being targeted therapeutically to inhibit autoreactive T cell trafficking, and these findings suggest that it may be possible simultaneously to target autoreactive or malignant cell survival.

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