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Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

ABSTRACT: Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

PROVIDER: PRJNA408016 | ENA |

REPOSITORIES: ENA

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Transcriptional signature of human pro-inflammatory TH17 cells [TH17 clones]

Project description:Human IL-10– and IL-10+ TH17 clones maintained their pro- or anti-inflammatory characteristics after long-term culture. There were similarities between human IL-10– vs. IL-10+ TH17 clones and mouse pathogenic vs. non-pathogenic TH17 cells.

2017-09-29 | GSE104023 | GEO

Transcriptional signature of human pro-inflammatory TH17 cells

Project description:Transcriptional signature of human pro-inflammatory TH17 cells

| PRJNA407976 | ENA

Transcriptional signature of human pro-inflammatory TH17 cells [ex vivo TH17 cells]

Project description:Transcriptional signature of human pro-inflammatory TH17 cells [ex vivo TH17 cells]

| PRJNA407982 | ENA

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

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

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

| PRJNA625315 | ENA

Transcriptional signature of human pro-inflammatory TH17 cells [ex vivo TH17 cells]

Project description:Human peripheral blood IFN-γ+IL-17+ (TH1/17) and IFN-γ–IL-17+ (TH17) CD4+ T cells display distinct transcriptional profiles in high-throughput transcription analyses. Compared to TH17 cells, TH1/17 cells have similar gene signatures to mouse pathogenic TH17 cells.

2017-09-29 | GSE104021 | GEO

Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis

Project description:This study aimed to assess the role of the CD5-CK2-STAT3 signalling axis in human pro-inflammatory Th17 cells. Blockade of CD5 reduced production of IL-17A, IFN-γ and GM-CSF by Th17-polarised cells without affecting proliferation. In comparison, blockade of its intracellular interaction partner CK2 exerted partly similar effects with a decrease in IL-17A and GM-CSF production but also impaired T cell proliferation. Both blocking agents resulted in a decreased phosphorylation of the downstream signalling molecule STAT3. The CD5 targeting treatment was able to abolish cytotoxic effects caused by Th17-polarised cells. Transcriptomic and proteomic analysis showed that CD5 expression correlates with an inflammatory immune profile in MS in serum as well as CSF.

2025-09-17 | GSE189998 | GEO

Autoimmunity and infection give rise to distict inflammatory Th17 subsets [bulk RNA-seq]

Project description:Th17 cells are a heterogeneous population that is critical for tissue homeostasis and inflammation during clearance of infections and autoimmunity. Despite substantial efforts distinguishing homeostatic and inflammatory roles of Th17 cells, the mechanism underlying the divergent functions of inflammatory Th17 cells is poorly understood. In this study, we show that the inflammatory Th17 engaged in autoimmune colitis and those involved in infection-induced colitis are two distinguishable populations illustrated by their distinct responses to a pharmacological molecule, clofazimine (CLF). Distinct from existing Th17 inhibitors, CLF selectively inhibits pro-autoimmune Th17 cells while preserving the functional state of infection-elicited Th17 cells through restricting Aldh1l2expression. Using bulk RNA sequencing, we explored transcriptional response to CLF on in vitro differentiated inflammatory and homeostatic Th17 cells. Notably, we identified a unique suppression in the transcription of signature inflammatory genes in Th17 cells with a marginal effect on those elicited by infection.

2023-06-13 | GSE234593 | GEO

Autoimmunity and infection give rise to distict inflammatory Th17 subsets [single-cell RNA-seq]

Project description:Th17 cells are a heterogeneous population that is critical for tissue homeostasis and inflammation during clearance of infections and autoimmunity. Despite substantial efforts distinguishing homeostatic and inflammatory roles of Th17 cells, the mechanism underlying the divergent functions of inflammatory Th17 cells is poorly understood. In this study, we show that the inflammatory Th17 engaged in autoimmune colitis and those involved in infection-induced colitis are two distinguishable populations illustrated by their distinct responses to a pharmacological molecule, clofazimine (CLF). Distinct from existing Th17 inhibitors, CLF selectively inhibits pro-autoimmune Th17 cells while preserving the functional state of infection-elicited Th17 cells through restricting Aldh1l2expression. Using single-cell RNA sequencing, we explored inflammatory Th17 transcriptional response to CLF from the colonic tissue of mice during autoimmune colitis and Citrobacter rodentiuminfection using Rorc gfp/+ reportor mice. Notably, we identified a unique suppression in the transcription of signature inflammatory genes in Th17 cells from autoimmune colitis with a marginal effect on those elicited by infection. Additionally, we illustrate with these data that the transcriptionally programming of pro-autoimmune Th17 cells are, indeed, unique compared to infection-elicited Th17 cells. Finally, we analyzed the impact of CLF on human inflammatory Th17 cells from the inflammed colon of a patient with IBD.

2023-06-13 | GSE234592 | GEO

Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis

Project description:Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis

| PRJNA785551 | ENA