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In vitro grown organoids treated with IFNγ mimicking in vivo intestinal crypts cells aging

ABSTRACT: In vitro grown organoids treated with IFNγ mimicking in vivo intestinal crypts cells aging

PROVIDER: PRJNA729241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14506964_1.fastq.gz	Fastqsanger.gz
	SRR14506964_2.fastq.gz	Fastqsanger.gz
	SRR14506965_1.fastq.gz	Fastqsanger.gz
	SRR14506965_2.fastq.gz	Fastqsanger.gz
	SRR14506966_1.fastq.gz	Fastqsanger.gz

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In vitro grown organoids treated with IFNγ mimicking in vivo intestinal crypts cells aging

Project description:Aging-related intestinal dysfunctions include loss of barrier integrity, altered stress responses, nutrient malabsorption, and cancer formation. Influence of aging on intestinal stem cell (ISC) and their niches can explain underlying causes for perturbation in ISC function during aging. However, molecular mechanisms for such decrease in functionality of ISCs during aging remain largely undetermined. Using different transcriptome-wide approaches including single-cell RNA-seq from intestinal crypt cells and immune cells of lamina propria, we characterized age-specific transcriptional programs in the intestinal epithelium. We found that aged ISCs strongly upregulate antigen presenting pathway genes and over-express secretory lineage marker genes leading to a compromised homeostasis of the intestinal epithelium. Mechanistically, increase of interferon gamma (IFNgamma) release by cytotoxic CD4 T cells and innate lymphoid type 2 cells (ILC2) in lamina propria of aged intestine lead to induction of Stat1 in ISCs that trigger MHC class II expression and prime them towards a secretory fate. Altogether these findings, clarify the cross talk between immune cells and ISC in aged intestine and identified the IFNgamma-Stat1-MHCII axis as the key gene network driving intestinal inflammaging phenotype and loss of tissue homeostasis. Our data provide basic and complementary knowledge for the development of therapeutic intervention for aging-related intestinal dysfunction and diseases.

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Project description:The cytokine IFNγ differentially impacts on tumors upon immune checkpoint blockade (ICB). Despite our understanding of downstream signaling events, less is known about 36 regulation of its receptor (IFNγ-R1). With an unbiased genome-wide CRISPR/Cas9 screen for critical regulators of IFNγ-R1 cell surface abundance, we identified STUB1 as an E3 ubiquitin ligase for IFNγ-R1 in complex with its signal-relaying kinase JAK1. STUB1 mediates ubiquitination-dependent proteasomal degradation of IFNγ-R1/JAK1 complex through IFNγ-R1K285 and JAK1K249. Conversely, STUB1 inactivation amplifies IFNγ signaling, sensitizing tumor cells to cytotoxic T cells in vitro. This was corroborated by an anticorrelation between STUB1 expression and IFNγ response in ICB-treated patients. Consistent with the context-dependent effects of IFNγ in vivo, anti-PD-1 response was increased in heterogenous tumors comprising both wildtype and STUB1-deficient cells but not full STUB1 knockout tumors. These results uncover STUB1 as a critical regulator of IFNγ-R1, and highlight the context-dependency of STUB1-regulated IFNγ signaling for ICB outcome.

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