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IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response [dataset 1]

ABSTRACT: IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response [dataset 1]

PROVIDER: PRJNA530540 | ENA |

REPOSITORIES: ENA

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Similar Datasets

IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response [dataset 2]

Project description:IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response [dataset 2]

| PRJNA530543 | ENA

IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response

Project description:IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response

| PRJNA530535 | ENA

IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response [dataset 2]

Project description:we define critical cell-type-specific contributions to the induction and effector mechanism of macrophage-driven colitis, as manifested in mice harboring IL-10R deficiencies and human IBD pathologies

2019-04-03 | GSE129212 | GEO

IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response [dataset 1]

2019-04-03 | GSE129211 | GEO

IL-23 producing IL-10Rα-deficient gut macrophages elicit an IL-22-driven pro-inflammatory epithelial cell response

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

2019-04-03 | GSE129215 | GEO

IL-23-producing IL-10R?-deficient gut macrophages elicit an IL-22-driven proinflammatory epithelial cell response.

Project description: Not available

| S-EPMC6697185 | biostudies-literature

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

Gene expression profiles in the ileal and colonic epithelial cells from Interleukin (IL)-23-deficient mice and IL-22-deficient mice

Project description:To investigate the function of IL-23 and IL-22 on the intestinal epithelial cells, we analyzed the gene expression profiles in ileal and colonic epithelial cells of mice deficient in IL-23 and IL-22.

2023-09-08 | GSE236445 | GEO

Differential role of IL-23 and IL-17 in intestinal regulation

Project description:Interleukin-23 (IL-23) and IL-17 are cytokines currently being targeted in clinical trials. Although inhibition of these cytokines is effective for treating psoriasis, IL-12/23 inhibition attenuates Crohn's disease, while IL-17A or IL-17RA inhibition exacerbates disease. This dichotomy between IL-23 and IL-17 was effectively modeled in the mdr1a- /- mouse model of colitis. IL-23 inhibition attenuated disease by decreasing colonic inflammation while enhancing Treg accumulation. Exacerbation of colitis by IL-17A or IL-17RA inhibition was associated with severe weakening of the intestinal epithelial barrier, culminating in increased colonic inflammation and accelerated mortality. These data show that IL-17A acts on intestinal epithelium to promote barrier function and provides insight into mechanisms underlying exacerbation of Crohn's disease when IL-17A or IL-17RA is inhibited.

2015-08-20 | GSE72212 | GEO

RNA-Seq analysis of IL-23 induced skin transcriptome

Project description:We performed RNA-Seq analysis and compared three groups 1) WT+IL-23 v. WT+GFP (control), 2) Mdl1-/-+IL-23 v. WT+GFP (control), and 3) WT+IL-23 v. Mdl1-/-+IL-23. Sets of differentially expressed genes (DEG) were defined on the basis of standard thresholds i.e. a |log2FC|≥2 combined with an adjusted p-value≤0.01 against the control group. Differential expression analysis revealed 1171 (619 up-regulated and 552 down-regulated) DEGs in WT+IL-23 v. WT+GFP, 414 (303 up-regulated and 111 down-regulated) DEGs in Mdl1-/-+IL-23 v. WT+GFP, and 260 (122 up-regulated and 138 down-regulated) DEGs in WT+IL-23 v. Mdl1-/-+IL-23

2022-07-02 | GSE133830 | GEO

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