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Pulmonary ILC2s differentially depend on epithelial cell- and lymphatic endothelial cell-IL-7 in acute and chronic airway inflammations

ABSTRACT: This study reveals the role of IL-7 produced by pulmonary stromal cells for the maintenance and activation of group 2 innate lymphoid cells (ILC2s) in the lung.

ORGANISM(S): Mus musculus

PROVIDER: GSE200372 | GEO | 2023/09/08

REPOSITORIES: GEO

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Pulmonary ILC2s differentially depend on epithelial cell- and lymphatic endothelial cell-IL-7 in acute and chronic airway inflammations

Project description:Pulmonary ILC2s differentially depend on epithelial cell- and lymphatic endothelial cell-IL-7 in acute and chronic airway inflammations

| PRJNA824340 | ENA

Proteome of group 2 innate lymphoid cells (ILC2s) stimulated with IL33 and TL1A

Project description:We analyzed the total proteome of group 2 innate lymphoid cells (ILC2s) after different stimulation with interleukin-33 (IL-33), a cytokine playing a critical role in human asthma, and TL1A, a TNF-family cytokine also known to activate ILC2s. Upon combined stimulation with IL-33 plus TL1A, we show that lung ILC2s produce high amounts of IL-9 and acquire a transient ‘ILC9’ phenotype. This phenotype is characterized by simultaneous production of large amounts of type 2 cytokines (IL-5, IL-13 and IL-9), induction of the IL-2 receptor CD25 (Il2ra), and of the transcription factors IRF4, JunB and BATF, that form immune-specific complexes known to induce IL-9 expression.

2024-03-05 | PXD041987 | Pride

ICOS-driven Cholesterol and Cortisol Biosynthesis Shape IL-10 Production in ILC2s to Regulate Airway Hyperreactivity

Project description:Group 2 innate lymphoid cells (ILC2) induce type 2 inflammation in the lungs in response to allergens. Here, we investigated the regulatory mechanism of IL-10 production by ILC2s on the development of airway hyperreactivity (AHR), with a particular focus on the role of ICOS. Our findings demonstrate that inhibition of ICOS in pulmonary ILC2s significantly promotes IL-10 production. Lack of ICOS reprograms ILC2 steroid metabolism, resulting in increased cholesterol and cortisol biosynthesis and Glucocorticoid receptor (GR) activation. Consequently, this reprogramming regulates MAF and NFIL3 activation, thereby promoting IL-10 production. We notably found that in vivo GR inhibition or ILC2-specific GR deficiency exacerbated the development of AHR in multiple mouse models. Finally, we extended our findings to a human setting and demonstrated concordant results between murine models and human ILC2s. Taken together, our results therefore indicate that ICOS negatively regulates IL-10 production in ILC2s by controlling cholesterol and cortisol biosynthesis.

2025-06-24 | GSE288711 | GEO

Expression data from naive, effector and memory-like ILC2s isolated from mouse lungs and those from effector and memory-like ILC2s isolated from mediastinal lymph node

Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naÃ¯ve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.

2016-06-30 | E-GEOD-81700 | biostudies-arrayexpress

Differential activation of human ILC2s by IL-25 and IL-33

Project description:The epithelial cell derived cytokines IL-25 and IL-33 can both activate type 2 innate lymphoid cells (ILC2s). It is not known whether the actions of these cytokines on ILC2s are similar or divergent. To investigate this we performed in vitro culture of human ILC2s with a variety of cytokine combinations including IL-2, IL-7, IL-25 and IL-33. Transcriptome profiling of these different condtions allowed us to assess the impact on gene expression of the different treatments. The results show that IL-25 and IL-33 promote divergent gene expression programs indicating that differential expression of these cytokines can cause diverse ILC2 effector function.

2017-08-01 | GSE72433 | GEO

Runx/Cbfβ complexes protect ILC2s from exhaustion during allergic airway inflammation

Project description:Group 2 innate lymphoid cells (ILC2s) have tissue-resident competence and contribute to the pathogenesis of allergic diseases. Therefore, there should be mechanisms to maintain the capacity of ILC2s to produce TH2 cytokines under chronic inflammatory conditions. Here, we report that Runx proteins are essential to prevent exaggerated activation of ILC2, in part by antagonizing GATA-3 function at steady state. However, during allergic inflammation, the absence of Runx in ILC2s impaired their ability to proliferate and produce effector TH2 cytokines and chemokines, but instead induced expression of T cell exhaustion markers including IL-10 and TIGIT. These exhausted ILC2s were unabale to induce type 2 immune responses against repeated allergen inhalation. Thus, Runx proteins protect ILC2s from exhaustion during continuous allergic inflammation.

2019-01-07 | GSE111871 | GEO

Activation-induced cell death of ILC2s via TIGIT suppresses chronic airway allergy

Project description:Chronic allergy induces TIGIT+ ILC2s at the sites of severe inflammation. To clearly isolate and follow the TIGIT+ ILC2s, we generated Tigit-Cre-ERT2: Rosa26-loxp-stop-loxp-tdTomato mice. tdTomato expression was induced in the TIGIT+ ILC2 of the mice by repeated intranasal administration of papain and oral tamoxifen treatment for 19 days. The tdTomato- and + ILC2s were sorted for RNA-seq and ATAC-seq analysis. We then performed gene expression profiling analysis using data obtained from RNA-seq of tdTomaoto- and + ILC2s. To call peaks, ATAC-seq data were aggregated by each unique cell type, and peak summits were called using HOMER.

2023-04-05 | GSE212180 | GEO

Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s)

Project description:Transcriptomal comparison between group 2 innate lymphoid cells (ILC2s) in the murine small intestine (SI-ILC2s) and those in white adipose tissue (WAT-ILC2s).

2019-07-02 | GSE130530 | GEO

Epigenome analyses implicate ILC2s as key mediators of allergic airway inflammation

Project description:Group 2 innate lymphoid (ILC2) cells are major producers of the cytokines that drive allergic asthma and elevated levels of ILC2s have been detected in the blood and sputum of asthma patients. Asthma susceptibility has strong (epi)genetic components, but the underlying mechanisms and whether they are linked to ILC2 biology remain unclear. To reveal the molecular basis of ILC2 function in allergic airway inflammation (AAI) and assess its relevance for understanding how genetic variation affects asthma susceptibility. Gata3-IRES-YFP reporter mice were used to isolate ILC2s from bronchoalveolar lavage fluid and lymph nodes. Human naive ILC2s were purified from peripheral blood and activated in vitro. We employed RNA-Seq, ChIPm-Seq and computational approaches to study the transcriptome and epigenome in the context of ILC2 activation, tissue-specific functions and genetic susceptibility to asthma. Activated ILC2s displayed a tissue-specific gene expression signature that emerged from a highly similar epigenome. We identify superenhancers - a class of regulatory regions susceptible to epigenetic drugs - controlling ILC2 identity and asthma-associated genes. The majority of genes implicated in asthma by genome-wide association studies resided in an active or primed state in ILC2s. A substantial number of asthma-associated genetic variants were found in ILC2 gene regulatory elements. Our genome-wide analyses reveal new potential functions for ILC2s in AAI, which possess a plastic and flexible epigenome. Importantly, we reveal a strong link between gene regulatory mechanisms in ILC2s and the (epi)genetic basis of asthma susceptibility, supporting a pathogenic role for ILC2s in human asthma.

2021-05-03 | GSE90641 | GEO

Piezo1 channels restrain ILC2s and regulate the development of airway hyperactivity [piezo1KO]

Project description:Mechanosensitive ion channels sense force and pressure in immune cells to drive the inflammatory response in highly mechanical organs. Here we report that Piezo1 channels repress group 2 innate lymphoid cells (ILC2s)-driven type 2 inflammation in the lungs. Piezo1 is induced on lung ILC2s upon activation, as genetic ablation of Piezo1 in ILC2s increases their function and exacerbates the development of airway hyperreactivity (AHR). Conversely, Piezo1 agonist Yoda1 reduces ILC2-driven lung inflammation. Mechanistically, Yoda1 inhibits ILC2 cytokine secretion and proliferation in a KLF2-dependent manner, as we further found that Piezo1 engagement reduces ILC2 oxidative metabolism. Consequently, in vivo Yoda1 treatment notably reduces the development of AHR in experimental models of ILC2-driven allergic asthma. Human circulating ILC2s express and induce Piezo1 upon activation, as Yoda1 treatment of humanized mice reduces human ILC2-driven AHR. Our studies define Piezo1 as a critical regulator of ILC2s and we propose the potential of Piezo1 activation as a novel therapeutic approach for the treatment of ILC2-driven allergic asthma.

2024-02-20 | GSE255882 | GEO

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