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Transcriptional analysis of human IL-23R mediated apoptosis in human cervical cancer cells in vitro

ABSTRACT: We found that IL-23R mediated HeLa cell apoptosis by characterizing the functional domains responsible for this event. For exploring apoptotic pathways activated by IL-23R, the altered transcriptomic profiles in responding to IL-23R over-expression was also revealed by RNAseq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE229036 | GEO | 2023/04/06

REPOSITORIES: GEO

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Bulk RNA-seq of interleukin-23 receptor (IL-23R) -deficient and IL-23R-sufficient colonic mouse regulatory T cells

Project description:To define the IL-23R-dependent changes in intestinal regulatory T cells (Treg cells) that might contribute to the impact on Treg cell function and selective advantage

2023-02-17 | GSE208621 | GEO

Candida albicans 23R

Project description:Candida albicans 23R genome sequencing project

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IL-23R signaling induces a colitogenic phenotype in Th1 cells.

Project description:IL-23R signaling induces a colitogenic phenotype in Th1 cells.

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Interleukin-23 receptor signaling in regulatory T cells in a mouse model of inflammation-associated cancer.

Project description:The pro-inflammatory cytokine interleukin-23 (IL-23) has been implicated in colorectal carcinogenesis (CRC). Yet, the cell-specific contributions of IL-23 receptor (IL-23R) signaling in CRC remain unknown. One of the cell types that highly expresses IL-23R are colonic regulatory T cells (Treg cells). The aim of this study was to define the contribution of Treg cell-specific IL-23R signaling in sporadic and inflammation-associated CRC. In mice, the role of IL-23R in Treg cells in colitis-associated cancer (CAC) was investigated using azoxymethane/dextran sodium sulphate in wild-type Treg cell reporter mice (WT, Foxp3YFP-Cre), and mice harboring a Treg cell-specific deletion of IL-23 (Il23rΔTreg). Il23rΔTreg mice had increased dysplasia compared to WT mice associated with decreased tumor-infiltrating macrophages. The role of Treg cell IL-23R in sporadic CRC was examined via orthotopic injection of the syngeneic colon cancer cell line MC-38 submucosally into the colon/rectum of mice. In the sporadic cancer model, Il23rΔTreg mice had increased survival and decreased tumor size compared to WT mice. Additionally, MC-38 tumors of Il23rΔTreg mice had a higher frequency of pro-inflammatory macrophages and IL-17 producing CD4+ T cells. This data suggests that loss of IL-23R signaling in Treg cells permits IL-17 production by CD4+ T cells that in turn promotes pro-inflammatory macrophages to clear tumors. These findings further support and highlight the importance of selecting a physiologically relevant model based on the type of cancer in which to evaluate the role of specific genes in late tumorigenesis. Finally, single-cell RNA-seq analysis of a previously published dataset in human sporadic cancer, revealed that IL23R was highly expressed in CRC compared to other cancers and specifically in tumor-associated Treg cells.

2024-02-28 | GSE240707 | 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]

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

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

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

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

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Induction of pathogenic Th17 cells by salt inducible kinase SGK-1 (SGK-1 KO)

Project description:Th17 cells are highly proinflammatory cells that are critical for clearing extracellular pathogens like fungal infections and for induction of multiple autoimmune diseases1. IL-23 plays a critical role in stabilizing and endowing Th17 cells with pathogenic effector functions2. Previous studies have shown that IL-23 signaling reinforces the Th17 phenotype by increasing expression of IL-23 receptor (IL-23R)3. However, the precise molecular mechanism by which IL-23 sustains the Th17 response and induces pathogenic effector functions has not been elucidated. Here, we used unbiased transcriptional profiling of developing Th17 cells to construct a model of their signaling network and identify major nodes that regulate Th17 development. We identified serum glucocorticoid kinase-1 (SGK1), as an essential node downstream of IL-23 signaling, critical for regulating IL-23R expression and for stabilizing the Th17 cell phenotype by deactivation of Foxo1, a direct repressor of IL-23R expression. A serine-threonine kinase homologous to AKT4, SGK1 has been associated with cell cycle and apoptosis, and has been shown to govern Na+ transport and homeostasis5, 6 7, 8. We here show that a modest increase in salt (NaCl) concentration induces SGK1 expression, promotes IL-23R expression and enhances Th17 cell differentiation in vitro and in vivo, ultimately accelerating the development of autoimmunity. The loss of SGK1 resulted in abrogation of Na+-mediated Th17 differentiation in an IL-23-dependent manner. These data indicate that SGK1 is a critical regulator for the induction of pathogenic Th17 cells and provides a molecular insight by which an environmental factor such as a high salt diet could trigger Th17 development and promote tissue inflammation. Th17 cells; comparing Sgk1-/- to WT

2013-03-07 | E-GEOD-43956 | biostudies-arrayexpress

Induction of pathogenic Th17 cells by salt inducible kinase SGK-1 (NaCl)

2013-03-07 | E-GEOD-43957 | biostudies-arrayexpress

MicroRNA-155 confers encephalogenic potential to Th17 cells by promoting IL-23 responsiveness and effector gene expression

Project description:We examined the role of miR-155 in differentiated Th17 cells during their induction of Experimental Autoimmune Encephalomyelitis (EAE). Using adoptive transfer experiments, we found that highly purified, MOG antigen specific Th17 cells lacking miR-155 are defective in their capacity to cause EAE. Gene expression profiling of purified miR-155-/- IL-17F+ Th17 cells identified a subset of effector genes that are dependent upon miR-155 for their proper expression through a mechanism involving repression of the transcription factor Ets1. Among the genes reduced in the absence of miR-155 was IL-23R, resulting in miR-155-/- Th17 cells being hypo-responsive to IL-23. Taken together, our study demonstrates a critical role for miR-155 in Th17 cells as they unleash autoimmune inflammation, and finds that this occurs through a signaling network involving miR-155, Ets1 and the clinically relevant IL-23-IL-23R pathway. two biological replicates of miR-155-/- CD4+ IL-17F RFP+ T cells compared to two biological replicates of miR-155+/+CD4+IL-17F RFP+ T cells (as a control).

2013-05-01 | E-GEOD-45122 | biostudies-arrayexpress

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