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

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

PROVIDER: PRJNA407982 | ENA |

REPOSITORIES: ENA

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

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

| PRJNA408016 | 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

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

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 profilling of In vitro-primed C.rodentium-specific Th17 cells, cytokine-differentiated Th17 cells and ex vivo Th17 cells following C.rodentium infection

Project description:Introduction: We reported a in vitro pathogen-specific priming system to using pathogen lysate stimulated splenic CD11c+ DCs to differentiate pathogen-specific murine T helper cells. This method allowed us to compare side-by-side transcriptional profiles of bulk T helper cells that are specific to distinct pathogens and to study their composition and functionality. Moreover, we can utilize cytokine reporter mice to isolate specific Th subtypes from these in vitro-primed T cells and study their transcriptional regulation. Method: We isolate commited Th17 cells by utilizing IL-17A fate-mapping mice (Il17aCRE; R26tdT). We generated Th17 cells in 3 conditions: 1. We used Cr-stimulated DCs to prime Th17 cells and sorted CD90+CFSE-tdT+ population, dubbed 'ppTh17' cells. CFSE+CD90+ naive T cells from the same culture as controls. 2. We polarized naive Il17aCRE; R26tdT CD4 T cells to Th17 lineage using previously defined cytokine and antibody cocktail (IL-6+TGFb1+IL-1b+IL-23; plate bound anti-CD3+anti-CD28). We sorted CD90+tdT+ population, dubbed 'cdTh17' cells. 3. We intragastrically infected Il17aCRE; R26tdT mice with 5x10^8 C.rodentium and harvested mesenteric lymph nodes at 10 days post infection (dpi). We sorted tdT+ CD4 T cells from mesenteric lymph nodes, dubbed "ex vivo Th17' cells. The four sorted populations were subjected to mRNA-sequencing analysis. Conclusion: We found that compared to cdTh17 cells, ppTh17 cells and ex vivo Th17 cells resemble each other. These two physiologically relevant Th17 populations maintain high levels of heterogeneity and plasticity, as well as posess ability to upregulate memory T cell related genes. cdTh17 cells highly express glycolysis and one-carbon metabolism genes, correlate with their expression of cell cycle genes, suggesting a highly activated state.

2020-01-10 | GSE141061 | GEO

Transcriptional profilling of In vitro-primed C.rodentium-specific Th17 cells, cytokine-differentiated Th17 cells and ex vivo Th17 cells following C.rodentium infection

Project description:Transcriptional profilling of In vitro-primed C.rodentium-specific Th17 cells, cytokine-differentiated Th17 cells and ex vivo Th17 cells following C.rodentium infection

| PRJNA591908 | ENA

Mouse Th17 T cells, IL-23 stimulated

Project description:Interleukin 23 (IL-23) triggers pathogenic features in pro-inflammatory, IL-17-secreting T cells (Th17 and Tγδ17) that play a key role in the development of inflammatory diseases. However, the IL-23 signaling cascade remains largely undefined. Here we used quantitative phosphoproteomics to characterize IL-23 signaling in primary murine Th17 cells. We quantified 6,888 phosphorylation sites in Th17 cells, and found 168 phosphorylations regulated upom IL-23 stimulation. IL-23 increased the phosphorylation of the myosin regulatory light chain (RLC), an actomyosin contractibility marker, in Th17 and Tγδ cells. IL-23-induced RLC phosphorylation required JAK2 and ROCK catalytic activity, and the study of the IL-23/ROCK axis revealed an unexpected role of IL-23 in the migration of Tγδ17 and Th17 cells. Moreover, pharmacological inhibition of ROCK reduced Tγδ17 recruitment to inflamed skin upon challenge with inflammatory agent Imiquimod. This work: i) provides new insights into phosphorylation networks that control Th17 cells, ii) widely expands the current knowledge on IL-23 signaling, and iii) contributes to the increasing list of immune cells subsets characterized by global phosphoproteomic approaches.

2020-03-25 | PXD016633 | Pride

Expression data from in vitro and ex vivo Th1- and Th17-polarized TRP1 TCR transgenic CD4+ cells

Project description:Serial comparison between Th1 and Th17 tumor-specific cells cultured in vitro and ex vivo after transferred into sublethaly irradiated B6.PL mice. Th17-derived cells acquire Th1-like properties in vivo but maintain a distinct molecular profile.

2011-12-17 | GSE26030 | GEO

The intestine harbours functionally distinct tissue-resident and inflammatory Th17 cells

Project description:Th17 cells are extensively studied because of their known pathogenic role in many inflammatory diseases, but are also important to support the integrity of the intestinal barrier in a non-inflammatory manner. Since therapeutic targeting of Th17 cell mediated pathologies carries the risk of inadvertently affecting protective Th17 cells, we set out to define the major distinctions between homeostatic tissue-resident Th17 cells and Th17 cells engaged in inflammatory reactions, focusing on the gut. We show here that homeostatic Th17 cells exhibit little plasticity towards expression of inflammatory cytokines, are characterised by a metabolism typical for quiescent or memory T cells, and do not participate in inflammatory processes. Infection-induced Th17 cells, on the other hand, show extensive plasticity towards pro-inflammatory cytokines, disseminate widely into the periphery and engage aerobic glycolysis in addition to oxidative phosphorylation typical for inflammatory effector cells.

2019-06-28 | GSE130302 | GEO

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