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Exploration of the activation process of Group 2 innate lymphoid cell (ILC2) isolated from mouse fat tissues to produce type 2 cytokine [mouse]

ABSTRACT: To investigate the gene expression underlying the activation process of ILC2, we performed time-series measurements of type 2 cytokine secretion activity (IL-5 or IL-13) of ILC2 from mouse fat tissues after IL-2/IL-33 stimulation . Single cells were collected separately before stimulation (Pre-stimulation), just after exhibiting type 2 cytokine secretion (Transition state), and secretion-positive (Activated state) or secretion-negative (Silent state) after sufficient time from stimulation, and performed RNA-seq on each cell for gene expression profiling analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE222762 | GEO | 2023/09/13

REPOSITORIES: GEO

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Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from human peripheral blood

Project description:To investigate the gene expression underlying the intercellular diversity in type 2 cytokine secretion activity of ILC2, we performed time-series measurements of type 2 cytokine secretion activity of ILC2 from human peripheral blood after IL-2/IL-33/TSLP stimulation . Single cells were collected separately before stimulation, in transition state or activated cells after stimulation, and performed RNA-seq on each cell for gene expression profiling analysis.

2023-09-13 | GSE222761 | GEO

Exploration of specific gene expression behind the intercellular heterogeneity of type 2 cytokine secretion activity of Group 2 innate lymphoid cell (ILC2) isolated from peripheral blood of severe asthma patients I

Project description:To investigate the gene expression underlying the intercellular diversity in type 2 cytokine secretion activity of ILC2, we performed time-series measurements of type 2 cytokine secretion activity of ILC2 from the peripheral blood of severe asthma patients after IL-33 stimulation . Single cells were collected separately before stimulation and secretion-negative or -positive cells after stimulation, and performed RNA-seq on each cell for gene expression profiling analysis.

2023-09-13 | GSE213810 | GEO

Expression data of ILC2 cells from Ets1-deleted and littermate control mice

Project description:The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2 ILC2 cells isolated from ETS1-deleted or litter mate control mice were cultured on OP9-DL1 with IL-7 and IL-33. Subsequently, RNA from ICOS+ cells was extracted, labelled and hybridized to Affymetrix microarrays. The goal of this study is to investigate ETS1-dependent genes in developing ILC2 cells.

2016-04-01 | E-GEOD-79742 | biostudies-arrayexpress

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.

2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress

Amino acid availability acts as a metabolic rheostat to determine the magnitude of ILC2 responses - WT ILC2

Project description:Group 2 innate lymphoid cells (ILC2) are functionally poised, tissue-resident lymphocytes that respond rapidly to damage and infection at mucosal barrier sites. ILC2 reside within complex microenvironments where they are subject to cues from both the diet and invading pathogens – including helminths. Emerging evidence suggests ILC2 are acutely sensitive not only to canonical activating signals, but also perturbations in nutrient availability. In the context of helminth infection, we identify amino acid availability as a nutritional cue in regulating ILC2 responses. ILC2 were found to be uniquely pre-primed to import amino acids via the large neutral amino acid transporters Slc7a5 and Slc7a8. Cell-intrinsic deletion of these transporters individually impaired ILC2 expansion, while concurrent loss of both transporters markedly impaired the proliferative and cytokine producing capacity of ILC2. Moreover, amino acid determined the magnitude of ILC2 responses in part via tuning of mTOR. These findings implicate essential amino acids as a metabolic requisite for optimal ILC2 responses within mucosal barrier tissues.

2022-12-22 | PXD038792 | Pride

The neuropeptide Neuromedin U stimulates innate lymphoid cells and promotes type 2 inflammation [ILC2 and ILC3]

Project description:The type 2 cytokines interleukin (IL)-4, IL-5, IL-9 and IL-13 play critical roles in stimulating innate and adaptive immune responses required for resistance to helminth infection and promotion of allergic inflammation, metabolic homeostasis and tissue repair. Group 2 innate lymphoid cells (ILC2s) are a potent source of type 2 cytokines and while significant advances have been made in understanding the cytokine milieu that promotes ILC2 responses, there are fundamental gaps in knowledge regarding how ILC2 responses are regulated by other stimuli. In this report, we demonstrate that ILC2s in the gastrointestinal tract co-localize with cholinergic neurons that express the neuropeptide neuromedin U (NMU). In contrast to other hematopoietic cells, ILC2s selectively express the NMU receptor 1 (NMUR1). In vitro stimulation of ILC2s with NMU induced rapid cell activation, proliferation and secretion of type 2 cytokines IL-5, IL-9 and IL-13 that was dependent on cell-intrinsic expression of NMUR1 and Gaq protein. In vivo administration of NMU triggered potent type 2 cytokine responses characterized by ILC2 activation, proliferation and eosinophil recruitment that was associated with accelerated expulsion of the gastrointestinal nematode Nippostrongylus brasiliensis or induction of lung inflammation. Conversely, worm burden was higher in Nmur1-/- mice compared to control mice. Further, use of gene-deficient mice and adoptive cell transfer experiments revealed that ILC2s were necessary and sufficient to mount NMU-elicited type 2 cytokine responses. Together, these data indicate that the NMU-NMUR1 neuronal signaling circuit provides a selective and previously unrecognized mechanism through which the enteric nervous system and innate immune system integrate to promote rapid type 2 cytokine responses that can induce anti-microbial, inflammatory and tissue-protective type 2 responses at mucosal sites.

2017-08-18 | GSE101623 | GEO

Identification of N6-methyladenosine (m6A) modified RNA in activated ILC2

Project description:Innate lymphoid cells (ILCs) are able to directly respond to alarmin signals and produce an array of effector molecules for immune protection and tissue homeostasis. However, how posttranscriptional machinery in ILCs execute extracellular stimuli towards robust gene expression is yet to understand. Here, we reported a cell type-specific role of N6-methyladenosine (m6A) RNA methylation in ILCs. Inducible deletion of m6A methyltransferase METTL3 had little impact on ILC maintenance in the steady state or cytokine-induced ILC1 or ILC3 activation, but dramatically diminished IL-25-triggered ILC2 response. Specific deletion of Mettl3 in ILC2 significantly attenuated cell expansion, cytokine production, inter-organ migration, and anti-helminth immunity. To investigate the molecular mechanism by which m6A modification regulates ILC2 response, we subjected IL-25-activated iILC2 to a m6A-tagged mRNA immunoprecipitation sequencing (meRIP-seq) to identify the m6A modified mRNA.

2023-06-26 | GSE207292 | GEO

Blocking CD226 regulates ILC2 effector function and alleviates airway hyperreactivity

Project description:Type 2 innate lymphoid cells (ILC2s) play a pivotal role in type 2 asthma. CD226 is a costimulatory molecule involved in various inflammatory diseases. Here, we aimed to investigate CD226 expression and function within human and mouse ILC2s, and to assess the impact of targeting CD226 on ILC2-mediated airway hyperreactivity (AHR). Our findings demonstrated an inducible expression of CD226 in activated ILC2s, enhancing their cytokine secretion and effector functions. Blocking CD226 ameliorates ILC2-dependent AHR in IL-33 and Alternaria Alternata-induced models. Interestingly, CD226 is expressed and inducible in human ILC2s, and its blocking reduces cytokine production. Finally, we showed that peripheral ILC2s in asthmatic patients exhibited elevated CD226 expression compared to healthy controls.Our findings underscore the potential of CD226 as a novel therapeutic target in ILC2s, presenting a promising avenue for ameliorating AHR and allergic asthma.

2024-04-16 | GSE264060 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of the effects of IL-10 production on sorted mouse pulmonary ILC2 Transcriptomes.

Project description:ILC2s are the dominant innate lymphoid cell population in the lungs at steady state and their release of type-2 cytokines is a central driver in responding eosinophil infiltration and increased airway hyperreactivity (AHR). For the first time, our laboratory has identified a unique subset of ILC2s in the lungs that produces and secretes IL-10, an anti-inflammatory cytokine, upon stimulation with IL-4. Overall this study introduces a novel, IL-4-inducible IL-10-producing population of ILC210s in the lung are naturally present in a high Th2 model of murine asthma. This research introduces a novel, cell-based immunotherapeutic potential of ILC210s that can be modulated by the signlaing transcription factors Blimp-1 and cMAF, as well as by glucose availability, opening new avenues for the treatment of ILC2-dependent airway inflammation.

2020-10-05 | GSE158983 | GEO

Identification of N6-methyladenosine (m6A) modified RNA in ILC2 of WT and Mettl3 Klrg1Cre mice

Project description:Innate lymphoid cells (ILCs) are able to directly respond to alarmin signals and produce an array of effector molecules for immune protection and tissue homeostasis. However, how posttranscriptional machinery in ILCs execute extracellular stimuli towards robust gene expression is yet to understand. Here, we reported a cell type-specific role of N6-methyladenosine (m6A) RNA methylation in ILCs. Inducible deletion of m6A methyltransferase METTL3 had little impact on ILC maintenance in the steady state or cytokine-induced ILC1 or ILC3 activation, but dramatically diminished IL-25-triggered ILC2 response. Specific deletion of Mettl3 in ILC2 significantly attenuated cell expansion, cytokine production, inter-organ migration, and anti-helminth immunity. To investigate the molecular mechanism by which m6A modification regulates ILC2 response, we subjected ILC2 of WT and Mettl3 Klrg1Cre mice to a m6A-tagged mRNA immunoprecipitation sequencing (meRIP-seq) to identify the m6A modified mRNA.

2023-06-26 | GSE223082 | GEO

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