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Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

ABSTRACT: Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

PROVIDER: PRJNA706749 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13859800_1.fastq.gz	Fastqsanger.gz
	SRR13859800_2.fastq.gz	Fastqsanger.gz
	SRR13859801_1.fastq.gz	Fastqsanger.gz
	SRR13859801_2.fastq.gz	Fastqsanger.gz
	SRR13859802_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

Project description:CD4+ T helper 17 (TH17) cells protect barrier tissues but also trigger autoimmunity. The mechanisms behind these opposing processes remain unclear. Here, we found that the transcription factor EGR2 controlled the transcriptional program of pathogenic TH17 cells in the central nervous system (CNS) but not that of protective TH17 cells at barrier sites. EGR2 was significantly elevated in myelin-reactive CD4+ T cells from patients with multiple sclerosis and mice with autoimmune neuroinflammation. The EGR2 transcriptional program was intricately woven within the TH17 cell transcriptional regulatory network and showed high interconnectivity with core TH17 cell-specific transcription factors. Mechanistically, EGR2 enhanced TH17 cell differentiation and myeloid cell recruitment to the CNS by upregulating pathogenesis-associated genes and myelomonocytic chemokines. T cell-specific deletion of Egr2 attenuated neuroinflammation without compromising the host’s ability to control infections. Our study shows that EGR2 regulates tissue-specific and disease-specific functions in pathogenic TH17 cells in the CNS.

2021-05-19 | GSE168288 | GEO

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

2023-06-28 | GSE224960 | GEO

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

2023-06-28 | GSE226795 | GEO

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

Project description:Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

| PRJNA933183 | ENA

Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

Project description:Transcription factor EGR2 controls homing and pathogenicity of TH17 cells in the central nervous system.

| PRJNA941799 | ENA

Activin-A limits Th17 pathogenicity and autoimmune neuroinflammation via CD39 and CD73 ectonucleotidases and Hif1-α -dependent pathways

Project description:In multiple sclerosis (MS), Th17 cells are critical drivers of autoimmune central nervous system (CNS) inflammation and demyelination. Th17 cells exhibit functional heterogeneity fostering both pathogenic and non-pathogenic, tissue-protective functions. Still, the factors that control Th17 pathogenicity remain incompletely defined. Here, using experimental autoimmune encephalomyelitis (EAE), an established mouse MS model, we report that therapeutic administration of activin-A ameliorates disease severity and alleviates CNS immunopathology and demyelination, associated with decreased activation of Th17 cells. In fact, activin-A signaling through activin-like kinase (ALK)4 receptor represses pathogenic transcriptional programs in Th17-polarized cells, while it enhances anti-inflammatory gene modules. Whole genome profiling and in vivo functional studies revealed that activation of the ATP-depleting CD39 and CD73 ectonucleotidases is essential for activin-A-induced suppression of the pathogenic signature and the encephalitogenic functions of Th17 cells. Mechanistically, aryl hydrocarbon receptor, along with STAT3 and c-Maf, are recruited to promoter elements on Entpd1 and Nt5e (encoding CD39 and CD73, respectively) and other anti-inflammatory genes, and control their expression in Th17 cells in response to activin-A. Notably, we show that activin-A negatively regulates the metabolic sensor, hypoxia-inducible factor-1 and key inflammatory proteins linked to pathogenic Th17 cell states. Of translational relevance, we demonstrate that activin-A is induced in the CNS of individuals with MS and restrains human Th17 cell responses. These findings uncover activin-A as a novel critical controller of Th17 cell pathogenicity that can be targeted for the suppression of autoimmune CNS inflammation.

2020-03-06 | GSE146439 | GEO

Sodium chloride generates anti-inflammatory Th17 cell responses but amplifies Th17 cell pathogenicity in pro-inflammatory cytokine microenvironments

Project description:T helper cells integrate signals from their microenvironment to acquire distinct specialization programs for efficient clearance of diverse pathogens or for immunotolerance. Ionic signals have recently been demonstrated to affect T cell polarization and function. Sodium chloride (NaCl) was proposed to accumulate in peripheral tissues upon dietary intake and to promote autoimmunity via the Th17 cell axis. Here we demonstrate that high NaCl conditions induced a stable, pathogen-specific, anti-inflammatory Th17 cell fate in human T cells in vitro. The p38/MAPK pathway, involving NFAT5 and SGK1, regulated FoxP3 and interleukin (IL)-17-expression in high-NaCl conditions. The NaCl-induced acquisition of an anti-inflammatory Th17 cell fate was confirmed in vivo in an experimental autoimmune encephalomyelitis (EAE) mouse model, which demonstrated strongly reduced disease symptoms upon transfer of T cells polarized in high NaCl conditions. However, NaCl was coopted to promote murine and human Th17 cell pathogenicity, if T cell stimulation occurred in a pro-inflammatory and TGF--low cytokine microenvironment. Taken together, our findings reveal a context-dependent, dichotomous role for NaCl in shaping Th17 cell pathogenicity. NaCl might therefore prove beneficial for the treatment of chronic inflammatory diseases in combination with cytokine-blocking drugs.

2020-04-15 | GSE148669 | GEO

RNA-seq of FR4+Egr2+, FR4+Egr2-, FR4-Egr2-, FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4 T cells

Project description:Transcription profiling of mouse FR4+Egr2+, FR4+Egr2- and FR4-Egr2- CD4+ T cells extracted from GFP-Egr2 knockin (Egr2 Kin) and FR4+Egr2-/-Egr3-/- and FR4-Egr2-/-Egr3-/- CD4+ T cells isolated from Egr2loxP/loxP hCD2-Cre Egr3-/- (Egr2/3 DKO) mice in the steady state or 21 days after infection with vaccinia virus.

2025-01-01 | E-MTAB-12736 | biostudies-arrayexpress

AMPK signaling downstream of adenosine 2A receptor represses Th17 cell pathogenicity through epigenetic and metabolic reprogramming.

Project description:Metabolic reprogramming controls protective or pathogenic Th17 cell responses; still, the precise molecular pathways that drive distinct immunometabolic states remain elusive. Here, we demonstrate that non-pathogenic Th17 cells induced by the immunoregulatory cytokine activin- A display reduced aerobic glycolysis and increased oxidative phosphorylation (OXPHOS). Notably, signaling through the adenosine A 2A receptor (A 2A R)/AMP-activated protein kinase (AMPK) axis in response to activin-A, boosts OXPHOS and reprograms pathogenic Th17 cells towards non-pathogenic states. Epigenetic studies revealed that pathogenic Th17 cells express highly the CBP/P300 binding protein (PCAF) which facilitates the acetylation of histone 3 at lysine 9 (H3K9ac) at genes related to the mammalian target of rapamycin complex 1 (mTORC1), glycolysis and Th17 pathogenicity programs. Instead, activin-A-treated Th17 cells display an AMPK-mediated suppression of PCAF activity and aerobic metabolism while, accumulate H3K9ac in gene loci related to OXPHOS. Collectively, we uncover A 2A R-AMPK as a central metabolic checkpoint that epigenetically regulates Th17 pathogenicity.

2025-09-27 | GSE284714 | GEO

Transcription factor EGR2 controls homing and pathogenicity of T<sub>H</sub>17 cells in the central nervous system.

Project description:CD4+ T helper 17 (TH17) cells protect barrier tissues but also trigger autoimmunity. The mechanisms behind these opposing processes remain unclear. Here, we found that the transcription factor EGR2 controlled the transcriptional program of pathogenic TH17 cells in the central nervous system (CNS) but not that of protective TH17 cells at barrier sites. EGR2 was significantly elevated in myelin-reactive CD4+ T cells from patients with multiple sclerosis and mice with autoimmune neuroinflammation. The EGR2 transcriptional program was intricately woven within the TH17 cell transcriptional regulatory network and showed high interconnectivity with core TH17 cell-specific transcription factors. Mechanistically, EGR2 enhanced TH17 cell differentiation and myeloid cell recruitment to the CNS by upregulating pathogenesis-associated genes and myelomonocytic chemokines. T cell-specific deletion of Egr2 attenuated neuroinflammation without compromising the host's ability to control infections. Our study shows that EGR2 regulates tissue-specific and disease-specific functions in pathogenic TH17 cells in the CNS.

| S-EPMC10500342 | biostudies-literature

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