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

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

PROVIDER: PRJNA530543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8836670.fastq.gz	Fastqsanger.gz
	SRR8836680.fastq.gz	Fastqsanger.gz
	SRR8836690.fastq.gz	Fastqsanger.gz
	SRR8836700.fastq.gz	Fastqsanger.gz
	SRR8836710.fastq.gz	Fastqsanger.gz

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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]

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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

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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: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

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

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

Project description:Cytokines maintain intestinal health, but precise intercellular communication networks remain poorly understood. Macrophages are immune sentinels of the intestinal tissue and are critical for gut homeostasis. Here, we show that in a murine inflammatory bowel disease (IBD) model based on macrophage-restricted interleukin-10 (IL-10) receptor deficiency (Cx3cr1Cre:Il10rafl/fl mice), proinflammatory mutant gut macrophages cause severe spontaneous colitis resembling the condition observed in children carrying IL-10R mutations. We establish macrophage-derived IL-23 as the driving factor of this pathology. Specifically, we report that Cx3cr1Cre:Il10rafl/fl:Il23afl/fl mice harboring macrophages deficient for both IL-10R and IL-23 are protected from colitis. By analyzing the epithelial response to proinflammatory macrophages, we provide evidence that T cells of colitic animals produce IL-22, which induces epithelial chemokine expression and detrimental neutrophil recruitment. Collectively, we define macrophage-specific contributions to the induction and pathogenesis of colitis, as manifested in mice harboring IL-10R deficiencies and human IBDs.

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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.

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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.

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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.

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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