Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The inhibitory receptor CD200R educates ILC1s for optimal cytotoxicity

ABSTRACT: Conventional natural killer (cNK) cells are educated through inhibitory receptor engagement with MHC-Ⅰ ligands, ensuring functional competence and self-tolerance. However, as a population likewise exhibiting cytotoxicity, whether type 1 innate lymphoid cells (ILC1s) undergo education and the underlying mechanisms remain unclear. Our study reveals that, CD200R, an inhibitory receptor specifically expressed by ILC1s, selectively suppresses ILC1 cytotoxicity upon CD200 engagement. Surprisingly, CD200R deficiency impairs ILC1 degranulation and cytotoxic activity without affecting inflammatory cytokine production. This defect is accompanied by compromised metabolic fitness in ILC1s. Analogous to cNK cell education, we demonstrate that CD200R educates ILC1 cytotoxicity primarily through the WNT/β-catenin pathway. Importantly, the impaired effector functions of uneducated ILC1s could be restored by exposure to certain cytokines. Collectively, our study defines a critical role for the inhibitory receptor CD200R in educating ILC1s to achieve cytotoxic maturity, revealing a parallel yet distinct mechanism from cNK cell education.

ORGANISM(S): Mus musculus

PROVIDER: GSE307477 | GEO | 2025/12/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The inhibitory receptor CD200R educates ILC1s for optimal cytotoxicity

Project description:The inhibitory receptor CD200R educates ILC1s for optimal cytotoxicity

| PRJNA1321790 | ENA

Heterogeneity of liver group 1 ILC1s

Project description:RNA sequencing demonstrated that liver Ly49E+ and Ly49E- ILC1s exhibited unique transcriptional profiles and phenotypic features. scRNA-seq analysis revealed heterogeneity within both cNK and ILC1 subsets in liver. cNK cells could be further divided into three clusters, which corresponded to different developmental stages. Ly49E expression could dissect ILC1s into two subsets: Ly49E+ ILC1s and Ly49E- ILC1s, which exhibited different functional characteristics.

2022-03-27 | GSE171851 | GEO

Prdm1 Positively Regulates Liver Group 1 ILCs Cancer Immune Surveillance and Preserves Functional Heterogeneity [RNA-Seq]

Project description:Group 1 innate lymphoid cells (ILCs) comprise conventional natural killer (cNK) cells and type 1 innate lymphoid cells (ILC1s). The main functions of liver cNK cells and ILC1s not only include directly killing target cells but also regulating local immune microenvironment of the liver through the secretion of cytokines. Uncovering the intricate mechanisms by which transcriptional factors regulate and influence the functions of liver cNK cells and ILC1s, particularly within the context of liver tumors, presents a significant opportunity to amplify the effectiveness of immunotherapies against liver malignancies. Using Ncr1-drived conditional knockout mouse model, our study reveals the regulatory role of Prdm1 in shaping the composition and maturation of cNK cells. Although Prdm1 did not affect the killing function of cNK cells in an in vivo cytotoxicity model, a significant increase in cancer metastasis was observed in Prdm1 knockout mice. Interferon-gamma (IFN-γ), granzyme B, and perforin secretion decreased significantly in Prdm1 deficient cNK cells and liver ILC1s. scRNA sequencing data also provided evidences that Prdm1 maintains functional subsets of cNK cells and liver ILC1s and facilitates communications between cNK cells, liver ILC1s and macrophages. The present study unveiled a novel regulatory mechanism of Prdm1 in cNK cells and liver ILC1s, showing promising potential for developing innovative immune therapy strategies against liver cancer.

2024-08-12 | GSE271380 | GEO

Prdm1 Positively Regulates Liver Group 1 ILCs Cancer Immune Surveillance and Preserves Functional Heterogeneity

2024-08-12 | GSE271233 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [scRNAseq_spleen_Ly49H+_steady-state]

Project description:Upon viral infection, NK cells expressing certain germline-encoded receptors are selected, expanded and maintained in an adaptive-like manner. Currently, these are thought to differentiate along a common pathway. However, by fate mapping of single NK cells upon murine cytomegalovirus (MCMV) infection, we identified two distinct NK cell lineages that contributed to adaptive-like responses. One was equivalent to conventional NK (cNK) cells while the other was transcriptionally similar to type 1 innate lymphoid cells (ILC1s). ILC1-like NK cells showed splenic-residency and strong cytokine production but also recognized and killed MCMV-infected cells, guided by activating receptor Ly49H. Moreover, they induced clustering of conventional type 1 dendritic cells and facilitated antigen-specific T cell priming early during MCMV infection, which depended on Ly49H and the NK cell-intrinsic expression of transcription factor Batf3. Thereby, ILC1-like NK cells bridge innate and adaptive viral recognition and unite critical features of cNK cells and ILC1s.

2021-08-25 | GSE180975 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [scRNAseq_spleen_LN_total_NK]

2021-08-25 | GSE180977 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [scRNAseq_Ly49H+_NK_retrogenic_spleen]

2021-08-25 | GSE180976 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [bulk_RNAseq_d8pi]

2021-08-25 | GSE180974 | GEO

Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection [bulk_RNAseq_steady_state]

2021-08-25 | GSE180973 | GEO

NKp46 regulates type 1 innate lymphoid cell proliferation and function and anti-acute myeloid leukemia activity

Project description:NKp46 is a critical regulator of natural killer (NK) cell immunity, but its function in non-NK innate immune cells remains unclear. Here, we show that NKp46 is indispensable for expressing IL-2 receptor-α (IL-2Rα) by non-NK liver-resident type-1 innate lymphoid cells (ILC1s). Deletion of NKp46 reduces IL-2Rα on ILC1s by downregulating NF-κB signaling, thus impairing ILC1 proliferation and cytotoxicity in vitro and in vivo. Likewise, the binding of anti-NKp46 antibody to NKp46 triggers the activation of NF-κB, the expression of IL-2Rα, interferon- γ (IFN-γ), tumor necrosis factor (TNF), proliferation, and cytotoxicity. Functionally, NKp46 expressed on mouse ILC1s interacts with tumor cells through cell–cell contact, increasing ILC1 production of IFN-γ and TNF, and enhancing cytotoxicity. In a mouse model of acute myeloid leukemia (AML), deletion of NKp46 impairs the ability of ILC1s to control tumor growth and reduces survival. This can be reversed by injecting NKp46+ ILC1s into NKp46 knock-out mice. Human NKp46+ ILC1s exhibit stronger cytokine production and cytotoxicity than their NKp46 counterparts, suggesting that NKp46 plays a similar role in humans. These findings identify an NKp46–NF-κB–IL-2Rα axis and suggest that activating NKp46 with an anti-NKp46 antibody, may provide a potential strategy for anti-tumor innate immunity.

2024-12-05 | GSE283199 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data