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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

ABSTRACT: ILC2 cells from mice cultured with or without hypoxia for indicated time period were analysed

ORGANISM(S): Mus musculus

PROVIDER: GSE196811 | GEO | 2022/05/25

REPOSITORIES: GEO

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Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer.

Project description:BackgroundPreviously, we uncovered a patient subgroup with highly malignant pancreatic cancer with serum markers CEA+/CA125+/CA19-9 ≥ 1000 U/mL (triple-positive, TP). However, the underlying immunosuppressive mechanism in the tumor immune microenvironment (TIME) of this subgroup is still unknown.MethodsHuman tissues were analyzed by flow cytometry, mass cytometry, and immunofluorescence staining. Mouse pancreatic ILC2s were expanded in vivo and used for RNA sequencing, chromatin immunoprecipitation (ChIP), and chemotaxis assays.FindingsThrough microarray data, we identified the accumulation of the hypoxia-induced factor-1α (HIF-1α) pathway in these TP patients. Via flow and mass cytometry, we discovered that a special subset of ILC2s were highly infiltrated in TP patients. Under the hypoxia microenvironment, ILC2s were found undergo a transition to a IL10+ regulatory phenotype, we named ILCregs which was correlated with pancreatic ductal adenocarcinoma (PDAC) progression. Further, neoadjuvant chemotherapy could ameliorate hypoxic tumor microenvironments so that significantly reverse the regulatory phenotype of ILCregs. Moreover, most tumor ILC2 were CD103-, which indicated its circulatory origin. The expression of Ccr2 was significantly upregulated on mouse ILCregs, and these cells selectively migrated to CCL2.InterpretationOur results indicate that the hypoxia microenvironment creates an immunosuppressive TIME by inducing ILCregs from a population of circulating group 2 ILCs in TP PDAC patients.FundingThis study was jointly supported by the National Natural Science Foundation of China (U21A20374, 82173091, and 81701630).

| S-EPMC9117270 | biostudies-literature

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [HMC-1]

Project description:Humans mast cell line-1 (HMC-1) cultured with or without hypoxia for indicated time period were analysed

2022-05-25 | GSE196810 | GEO

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

Project description:Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer [ILC2]

| PRJNA807349 | ENA

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer

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

2022-05-25 | GSE196812 | GEO

RNA-Seq of Group 2 innate lymphoid cells (ILC2) from lung and lymph node

Project description:Group 2 innate lymphoid cells (ILC2) promote the production of a type-2 immunological environment in the uterus and have tissue-specific gene signatures that change with pregnancy.

2023-04-15 | E-MTAB-5806 | biostudies-arrayexpress

RNA-Seq of Group 2 innate lymphoid cells (ILC2) from uterine tissue (Virgin, E9.5, E18.5)

2023-04-15 | E-MTAB-5803 | biostudies-arrayexpress

Evaluation of human group 2 innate lymphoid cells (ILC2) in Dengue Fever

Project description:Transcriptomic profiling of blood ILC2 from dengue fever patient groups and comparator healthy controls

2022-09-01 | GSE206648 | GEO

Group-2 Innate Lymphoid Cells Promote HCC Progression Through CXCL2-Neutrophil-Induced Immunosuppression.

Project description:Background and aimsDue to their inherent characteristics, the function of group-2 innate lymphoid cells (ILC2s) varies in a context-dependent manner. ILC2s are involved in certain liver diseases; however, their involvement in HCC is unknown. In the present study, we assessed the role of an HCC-derived ILC2 population in tumor progression.Approach and resultsThrough FACS and single-cell RNA sequencing, we discovered that ILC2s were highly enriched in human HCC and correlated significantly with tumor recurrence and worse progression-free survival as well as overall survival in patients. Mass cytometry identified a subset of HCC-derived ILC2s that had lost the expression of killer cell lectin-like receptor subfamily G, member 1 (KLRG1). Distinct from their circulating counterparts, these hepatic ILC2s highly expressed CD69 and an array of tissue resident-related genes. Furthermore, reduction of E-cadherin in tumor cells caused the loss of KLRG1 expression in ILC2s, leading to their increased proliferation and subsequent accumulation in HCC sites. The KLRG1- ILC2 subset showed elevated production of chemotaxis factors, including C-X-C motif chemokine (C-X-C motif) ligand (CXCL)-2 and CXCL8, which in turn recruited neutrophils to form an immunosuppressive microenvironment, leading to tumor progression. Accordingly, restoring KLRG1 in ILC2s, inhibiting CXCL2 in ILC2s, or depleting neutrophils inhibited tumor progression in a murine HCC model.ConclusionsWe identified HCC-associated ILC2s as an immune regulatory cell type that promotes tumor development, suggesting that targeting these ILC2s might lead to new treatments for HCC.

| S-EPMC8597094 | biostudies-literature

Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer

Project description:Hypoxia-reprogrammed regulatory group 2 innate lymphoid cells promote immunosuppression in pancreatic cancer

| PRJNA807345 | ENA

Enrichment of type I interferon signaling in colonic group 2 innate lymphoid cells in experimental colitis

Project description:Group 2 innate lymphoid cells (ILC2) are enriched in colonic tissues, but their precise role under intestinal inflammation, including inflammatory bowel disease (IBD) other than helminth infection, is poorly understood. Here, we analysed global gene expression of colonic ILC2 in healthy and colitis mice and found that type I interferon (T1IFN)-stimulated genes (ISGs) are enriched in ILC2 under DSS-induced colitis. Enhancement of T1IFN signaling in ILC2 under DSS-induced colitis were correlated to downregulation in cytokine production of ILC2, such as IL-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis both in wild-type and Rag2-deficient mice. Collectively, these findings show the potential roles of T1IFN in ILC2 contributing to the development of colitis.

2022-09-21 | GSE212939 | GEO

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