Cross-talk between ILC2 and Gata3high Treg locally constrains adaptive type 2 immunity
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ABSTRACT:
PROVIDER: PRJNA961816 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24302463_1.fastq.gz | Fastqsanger.gz | |||
| SRR24302463_2.fastq.gz | Fastqsanger.gz | |||
| SRR24302464_1.fastq.gz | Fastqsanger.gz | |||
| SRR24302464_2.fastq.gz | Fastqsanger.gz | |||
| SRR24302465_1.fastq.gz | Fastqsanger.gz |
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Project description:Regulatory T cells (Tregs) are essential for limiting adaptive immunity, and restrain type-2 inflammation in allergic disease. As Tregs function locally, the mechanisms that coordinate their suppressive role in the inflamed niche are of great interest. Here we show that group 2 innate lymphoid cells (ILC2) are critical mediators of IL-33-driven Treg expansion in allergic inflammation. ILC2-derived OX40L promotes the local expansion of Gata3high Tregs, which possess distinct transcriptional and functional programmes that enforce co-localisation with ILC2 in the inflamed airways. Using OX40 Treg-conditional mutant mice, we show that Gata3high Tregs are important for restraining adaptive type-2 immunity. Mechanistically, Gata3high Tregs modulate OX40L bioavailability on ILC2, which controls effector memory Th2 cell formation. As such, ILC2 can simultaneously engage both the effector and regulatory arms of adaptive type-2 immunity via the OX40L-OX40 signalling axis. More specifically, ILC2-Treg interactions serve as a critical feedback mechanism to control adaptive type-2 immunity.
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Project description:Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation
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Project description:Regulatory T cells (Tregs) are essential for limiting adaptive immunity, and restrain type-2 inflammation in allergic disease. As Tregs function locally, the mechanisms that coordinate their suppressive role in the inflamed niche are of great interest. Here we show that group 2 innate lymphoid cells (ILC2) are critical mediators of IL-33-driven Treg expansion in allergic inflammation. ILC2-derived OX40L promotes the local expansion of Gata3high Tregs, which possess distinct transcriptional and functional programmes that enforce co-localisation with ILC2 in the inflamed airways. Using OX40 Treg-conditional mutant mice, we show that Gata3high Tregs are important for restraining adaptive type-2 immunity. Mechanistically, Gata3high Tregs modulate OX40L bioavailability on ILC2, which controls effector memory Th2 cell formation. As such, ILC2 can simultaneously engage both the effector and regulatory arms of adaptive type-2 immunity via the OX40L-OX40 signalling axis. More specifically, ILC2-Treg interactions serve as a critical feedback mechanism to control adaptive type-2 immunity.
2024-07-19 | GSE230596 | GEO
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
Project description:Innate and adaptive lymphocytes work in concert to maintain tissue homeostasis and to mediate host defense at mucosal barriers. Herein, we used single cell analysis to show substantial diversity of gene expression in ILCs and T helper cells during a helminth infection in the lung. Notably, we found that the Calca gene, which is spliced to generate the neuropeptide CGRP, was selectively transcribed in ILC2s and Th2 cells in an activation dependent manner. The Calca locus acquired chromatin accessibility at the ILC2 precursor stage and is pre-programmed for rapid production of CGRP upon ILC2 activation. CGRP globally antagonized actions of neuromedin U (NMU) and the alarmin IL-33. However, CGRP selectively acted in concert with NMU and IL-33 to promote IL-5 expression, but not IL-13. The complex interplay among neuropeptides and alarmin fine-tunes type 2 immune responses and will undoubtedly become more relevant as therapeutic neuropeptide blockade advances in the clinic.
2019-06-25 | GSE131996 | GEO
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
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
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 | PXD038786 | Pride
Project description:Bulk RNA-seq of ILC2, Tconv, Th2, Treg Gata3hi and Treg Gatalo from the lungs of IL-33 treated mice
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