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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling [cytokine cultures]

ABSTRACT: RNA-sequencing of in vitro differentiated T cells cultured with varying cytokine conditions: IL-12, IL-12+IL-21, IL-1b+IL-6+IL-23, and TGFb+IL-6

ORGANISM(S): Mus musculus

PROVIDER: GSE202632 | GEO | 2022/05/11

REPOSITORIES: GEO

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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling [in vitro]

Project description:Single-cell RNA-sequencing of in vitro differentiated T cells cultured with IL-12+IL-21+IL-23 (Th1 cell condition) or IL-1b+IL-6+IL-23 (pathogenic Th17 cell condition)

2021-05-01 | GSE164518 | GEO

Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling

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

2021-05-01 | GSE164520 | GEO

Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling [in vivo]

Project description:Th1 cells were adoptively transferred into RAG1 KO mice from either wildtype (Il23rwt/eGFP) or KO (Il23reGFP/eGFP) donors. At the peak of disease in recipients of wildtype cells, the animals were euthanized and intestinal T cells were isolated from the chosen recipients of both wildtype and KO cells for 10x massively parallel single-cell RNA-sequencing.

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Induction of a colitogenic phenotype in Th1-like cells depends on interleukin-23 receptor signaling [cd160 knockout ex-vivo]

Project description:RNA-sequencing of wild-type and cd160 knockout CD4 T cells utilized in a T cell transfer colitis model

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Assessment of the impact of the IL23R R381Q variant in terms of IL-23-sensitive transcript induction

Project description:We stimulated T-cell blasts from IL23R R381Q homozygotes (n = 2), healthy controls homozygous for the ancestral allele (n = 9), homozygous individuals for TYK2 P1104A (n = 2) that selectively impairs responses to IL-23, and one patient each with autosomal recessive, complete TYK2 or IL-12Rb1 deficiency with IL-12, IL-23, IL-1b, and IL-1b plus IL-23 for 6 hours and performed RNA-sequencing. We used IL-1b as an IL-23-sensitizing agent as previously reported. We found that while T-cell blasts from IL23R R381Q homozygotes respond normally to IL-12 and IL-1b, their response to IL-23 and to IL-23 plus IL-1b is impaired

2023-01-13 | GSE216458 | GEO

The inflammasome-activated cytokine IL-1 is targeted for ubiquitylation and proteasomal degradation to limit its inflammatory potential

Project description:Interleukin-1B (IL-1B) is pathologically activated by inflammasome-associated caspase-1 in rare autoinflammatory conditions and in wide-spread diseases. Therefore, IL-1B activity must be fine-tuned to enable anti-microbial responses whilst limiting collateral damage. Here we report that, relative to other inflammasome components, IL-1B is rapidly turned over by the proteasome and this correlates with its decoration by K11-, K63- and K48-linked ubiquitin chains. This IL-1 degradation signal is not only a feature of inflammasome priming but is also triggered upon inflammasome activation. We demonstrate that IL-1 K133 is modified by ubiquitin and forms a salt bridge with IL-1B D129. Loss of IL-1 K133 ubiquitylation, or disruption of the K133:D129 electrostatic interaction, stabilizes IL-1Bprotein levels. Accordingly, IL-1B K133R/K133R mice display increased precursor IL-1Bupon inflammasome priming and increased bioactive IL-1B following inflammasome activation, both in vitro and following LPS injection in vivo. These findings reveal new mechanisms for limiting IL-1B activity and safeguarding against damaging inflammation.

2021-04-01 | PXD021305 | Pride

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [16S]

Project description:Acute gastrointestinal infection with intracellular pathogens like Salmonella Typhimurium triggers the release of the proinflammatory cytokine interleukin 1β (IL-1β). However, the role of IL-1β in intestinal defense against Salmonella remains unclear. Here, we show that IL-1b production is detrimental during Salmonella infection. Mice lacking IL-1b (IL-1b -/-) failed to recruit neutrophils to the gut during infection, which reduced tissue damage and prevented depletion of short-chain fatty acid-producing commensals. Changes in epithelial cell metabolism that typically support pathogen expansion, such as switching energy production from fatty acid oxidation to fermentation, were absent in infected IL-1b -/- mice which inhibited Salmonella expansion. Additionally, we found that IL-1b induces expression of complement anaphylatoxins and suppresses the complement-inactivator Carboxypeptidase N (CPN1). Disrupting this process via IL-1b loss prevented mortality in Salmonella-infected IL-1b -/- mice. Finally, we found that IL-1b expression correlates with expression of the complement receptor in patients suffering from sepsis, but not uninfected patients and healthy individuals. Thus, Salmonella exploits IL-1b signaling to outcompete commensal microbes and establish gut colonization. Moreover, our findings identify the intersection of IL-1b signaling and the complement system as key host factors involved in controlling mortality during invasive Salmonellosis.

2024-01-08 | GSE252070 | GEO

Salmonella manipulates the host to drive pathogenicity via induction of interleukin 1β [RNA-Seq]

2024-01-08 | GSE252069 | GEO

Cytokine receptor modulation by interleukin-2 broadly regulates T helper cell lineage differentiation

Project description:T helper (Th) cells control host defense to pathogens. IL 12R expression is required for Th1, IL-4Rα for Th2, and IL-6Rα/gp130 for Th17 differentiation to allow responsiveness to IL-12, IL-4, and IL-6, respectively. IL-2 via STAT5 controls Th2 differentiation by regulating the Th2 cytokine gene cluster and Il4ra expression. Here we show that IL-2 regulates Th1 differentiation, inducing STAT5-dependent IL-12Rβ2 and T-bet expression, with impaired human Th1 differentiation when IL-2 was blocked. Th1 differentiation was also impaired in mouse Il2-/- T cells but restored by IL-12Rβ2 expression. Consistent with IL-2’s inhibition of Th17 differentiation, IL-2 decreased Il6ra and Il6st/gp130 expression, and Il6st augmented Th17 differentiation even when IL-2 was present. Thus, IL-2 influences T-cell differentiation by modulating cytokine receptor expression to help specify/maintain differentiated states.

2011-04-24 | GSE27158 | GEO

IL-23R signaling induces a colitogenic phenotype in Th1 cells [cytokine cultures]

Project description:IL-23R signaling induces a colitogenic phenotype in Th1 cells [cytokine cultures]

| PRJNA836857 | ENA