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

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

PROVIDER: PRJNA530535 | ENA |

REPOSITORIES: ENA

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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 [dataset 1]

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

| PRJNA530540 | ENA

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

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

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 | GSE129211 | GEO

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

2019-04-03 | GSE129212 | 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

Transcription profiling of IL-22-/- samples

Project description:Infection by attaching and effacing (A/E) pathogens poses a serious threat to public health, as was highlighted by the recent outbreak of E. coli O157:H7 infection in the United States. Here, by using a murine A/E pathogen, Citrobacter rodentium, we demonstrate that C. rodentium infection is lethal to IL-22-/- mice within two weeks. IL-22, in the early phase of infection, is indispensable for preventing the invasion of bacteria through the intestinal epithelium, and thereby preventing systemic spread and mortality. We also show that IL-23 is required for the early induction of IL-22 during C. rodentium infection. Finally, our data suggest that IL-22 exerts its function by boosting the innate immune responses of colonic epithelial cells, especially though the induction of anti-microbial proteins, RegIIIÎ² and RegIIIÎ³. Experiment Overall Design: Control or IL-22-treated mouse colon in triplicate.

2008-04-07 | E-GEOD-10010 | biostudies-arrayexpress

RORγt inhibition selectively targets IL-17 producing human iNKT and γδ-T cells enriched in Spondyloarthritis while preserving IL-22 responses

Project description:Dysregulated IL-23/IL-17 responses have been linked to psoriatic arthritis and other forms of spondyloarthritides (SpA). RORγt, the key Thelper17 (Th17) cell transcriptional regulator, is also expressed by subsets of innate-like T cells, including invariant natural killer T (iNKT) and γδ-T cells, but how they contribute to disorders such as SpA is still unclear. Here we describe the presence of particular RORγt+T-betloPLZF- iNKT and γδ-hi T cell subsets in healthy peripheral blood. RORγt+ iNKT and γδ-hi T cells showed profound IL-23 mediated Th17-like immune responses and were clearly enriched within inflamed joints of SpA patients where they act as major IL-17 secretors. SpA derived iNKT and γδ-T cells showed a unique Th17 skewed phenotype and gene expression profile. Strikingly, RORγt inhibition blocked γδ17 and iNKT17 cell function while selectively sparing IL-22+ subsets. Overall, these findings highlight a unique diversity of human RORγt+ T cells and underscore the potential of RORγt antagonism to modulate aberrant type 17 responses.

2018-11-17 | GSE122624 | GEO

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