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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

Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity

Project description:Interleukin-23 receptor (IL-23R) signaling is critical for the generation of pro-inflammatory CD4+ IL-17-producing T cells (Th17) that can drive autoimmune tissue inflammation, but the underlying mechanisms are not clear. We integrated phosphoproteomic and transcriptomic data downstream of IL-23R and IL-12R, which share a common subunit, to identify mechanisms engaged specifically by IL-23. We identified chromodomain helicase DNA-binding protein 1 (CHD1), an epigenetic regulator, and the glucocorticoid receptor (GR), a transcription factor (TF), as mediators of IL-23R signaling. IL-23R activation promoted CHD1 interaction with TF STAT3 and co-binding at the TF RORγt locus to enforce a pro-inflammatory Th17 state. Conversely, IL-23R signaling altered phosphorylation of the GR, thereby preventing its activation and nuclear translocation, ultimately impairing GR-driven inhibition of pro-inflammatory Th17 gene programs. Our findings uncover two mechanisms by which IL-23 promotes a pro-inflammatory Th17 cell state, offering potential therapeutic targets for treating Th17-driven autoimmune tissue inflammation and restoring homeostasis.

2026-06-12 | PXD063778 | Pride

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

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

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

Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity I

2026-06-12 | GSE296187 | GEO

Interleukin-23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity II

2026-06-12 | GSE296401 | 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

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