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Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis

ABSTRACT: Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis

PROVIDER: PRJNA890323 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21898934_1.fastq.gz	Fastqsanger.gz
	SRR21898934_2.fastq.gz	Fastqsanger.gz
	SRR21898935_1.fastq.gz	Fastqsanger.gz
	SRR21898935_2.fastq.gz	Fastqsanger.gz
	SRR21898936_1.fastq.gz	Fastqsanger.gz

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Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [RNA-seq]

Project description:Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [RNA-seq]

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Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [ATAC-seq]

Project description:Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [ATAC-seq]

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Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [ATAC-seq]

Project description:Elucidate open chromatin regions associated with ChAT-GFP expression in in vitro polarized Th17 cells.

2022-11-13 | GSE215671 | GEO

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

Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis.

Project description:Experimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis (MS) in which Th17 cells have a crucial but unclear function. Here we show that choline acetyltransferase (ChAT), which synthesizes acetylcholine (ACh), is a critical driver of pathogenicity in EAE. Mice with ChAT-deficient Th17 cells resist disease progression and show reduced brain-infiltrating immune cells. ChAT expression in Th17 cells is linked to strong TCR signaling, expression of the transcription factor Bhlhe40, and increased Il2, Il17, Il22, and Il23r mRNA levels. ChAT expression in Th17 cells is independent of IL21r signaling but dampened by TGFβ, implicating ChAT in controlling the dichotomous nature of Th17 cells. Our study establishes a cholinergic program in which ACh signaling primes chronic activation of Th17 cells, and thereby constitutes a pathogenic determinant of EAE. Our work may point to novel targets for therapeutic immunomodulation in MS.

| S-EPMC9950465 | biostudies-literature

Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-13 | GSE215673 | 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

Cholinergic control of Th17 cell pathogenicity in experimental autoimmune encephalomyelitis [RNA-seq]

Project description:Elucidate a ChAT-associated gene expression program shared in ChAT-GFP-expressing splenic lymphocytes. (Seeking to answer the question, "Can we find a transcription factor that drives ChAT expression in lymphocytes?")

2022-11-13 | GSE215672 | GEO

Gene expression data from polarized T helper cells isolated from mice with opticospinal (OSE) experimental autoimmune encephalomyelitis (EAE)

Project description:T cells from the spleen of a mixed-gender pool of four double-transgenic 2D2 (TCRMOG) x IgHMOG mice (OSE) mice, which spontaneously develop experimental autoimmune encephalomyelitis (EAE), were used to derive TH1- and TH17-polarized cells, as described in https://doi.org/10.1371/journal.pone.0015531. Here, expression was compared, first, between TH1 and naïve TH0 and, second, between TH17 and naïve TH0 cells.

2020-08-21 | E-MTAB-9133 | biostudies-arrayexpress

Regulation of Th17 cell pathogenic function by miR-183/96/182

Project description:Th17 cells are key players in autoimmune diseases. However, the roles of non-coding RNAs in Th17 cells are largely unknown. Here, we show that deletion of the Dicer gene specifically in Th17 cells protects from experimental autoimmune encephalomyelitis (EAE). Th17 cells highly express the miR-183/96/182 cluster (miR-183C), in response to IL-6/STAT3 signaling. Moreover, miR-183C regulates pathogenic cytokine expression during Th17 development. Furthermore, transcription factor Foxo1 is one of functional targets of miR-183C in Th17 cells: Foxo1 negatively regulates the pathogenicity of Th17 cells and miR-183C represses Foxo1 expression. Collectively, our results demonstrate one of crucial roles for miR-183C cluster in regulation of Th17 cell function in autoimmune diseases.

2016-06-21 | GSE78505 | GEO

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