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RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis [Smart-seq]

ABSTRACT: To explore the downstream pathways of Rora regulation of memory ILC1 during memory maintenance period.

ORGANISM(S): Mus musculus

PROVIDER: GSE248316 | GEO | 2024/11/01

REPOSITORIES: GEO

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RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis

Project description:To explore the downstream pathways of Rora regulation of memory ILC1 during memory formation period.

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RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis [naïve]

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RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis [Smart-seq]

Project description:RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis [Smart-seq]

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RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis

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Project description:RORα is required for expansion and memory maintenance of ILC1s via a lymphnode-liver axis [naïve]

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RORα is crucial for attenuated inflammatory response to maintain intestinal homeostasis.

Project description:A member of the nuclear receptors, retinoic acid-related orphan receptor a (RORa) is an important transcription factor for various biological processes including circadian rhythm, metabolic regulation, immune cell development and cancer. Here we found that RORa is important for intestinal homeostasis by negatively regulating the transcriptional activity of NF-kB, a major inflammatory regulator in intestinal epithelial cells. Intestinal Rora-deficient mice found were highly susceptible to DSS-induced injury. Transcriptome analysis showed that intestine-specific Rora deletion causes regulatory impairment of NF-kB signaling leading to excessive inflammatory responses. RORa specifically binds to the NF-kB target promoter and inhibits transcriptional activity for transcriptional repression of NF-kB activity via histone deacetylase 3 (HDAC3). Taken together, RORa plays a pivotal role in the homeostatic regulation of intestinal epithelial cells in inflammatory conditions. Therefore, therapeutic strategies designed to modulate RORa activity may be beneficial in the treatment of chronic inflammatory diseases such as Inflammatory bowel disease (IBD).

2019-09-30 | GSE121977 | GEO

The inhibitory receptor CD200R educates ILC1s for optimal cytotoxicity

Project description: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.

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mRNA-sequencing of ILC1 cells

Project description:Purpose: To understanding the effects of RORa deficiency on ILC1 cells, we conducted bulk mRNA-seqencing Method: Firstly, we purified liver ILC1 cells (CD45.2+CD3-CD19-NKp46+NK1.1+CD49a+CD49b-) via Fluorescence Activated Cell Sorting, then frozen in -80 °C ultra-low temperature refrigerator, followed by High-throughput sequencing, in three replicates for WT (Rorafl/fl) mice and one replicate for cKO (Ncr1Cre-Rorafl/fl) , using Illumina Hiseq 1500 platform.

2022-09-28 | GSE186193 | GEO

Heterogeneity of liver group 1 ILC1s

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