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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Bulk RNA-Seq of lung Type 2 Innate Lymphoid cells (ILC2) in response to Alternaria alternata

ABSTRACT: Type 2 Innate Lymphoid cells (ILC2) play a crucial role in allergic airway inflammation. To identify transcriptional differences between naive ILC2 and allergen induced ILC2, mice were challenged with PBS control or Alternaria alternate on days 0, 3, 6 and 13. On day 14 ILC2 were isolated, sort-purified and sequenced.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Christoph Wilhelm

PROVIDER: E-MTAB-15967 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Bulk RNA-Seq of lung Type 2 Innate Lymphoid cells (ILC2) in response to papain

Project description:Type 2 Innate Lymphoid cells (ILC2) play a crucial role in allergic airway inflammation. To identify transcriptional differences between naive ILC2 and allergen induced ILC2, mice were challenged with PBS control or papain on days 0, 3, 6 and 13. On day 14 ILC2 were isolated, sort-purified and sequenced.

2025-12-10 | E-MTAB-15989 | biostudies-arrayexpress

Unconventional ST2- and CD127-negative lung ILC2 populations are induced by Alternaria

Project description:Background: Alternaria exposure is associated with severe asthma in humans. Alternaria exposure in mice potently activates group 2 innate lymphoid cells (ILC2s) via the IL-33/ST2 axis and causes ILC2s to robustly secrete type 2 cytokines. Objective: Our aim was to determine whether conventionally used ILC2 markers, ST2 (IL-33R) and CD127 (IL-7Ra), were sufficient to identify all Th2-cytokine producing ILCs after Alternaria exposure. Methods: Mice received intranasal Alternaria for three days prior to analysis. Lung ILCs were identified by flow cytometry as CD45+Lineage−Thy1.2+ lymphocyte-sized cells, divided into four subsets based on ST2 and CD127 expression, and stained for intracellular cytokines and transcription factors. Sort-purified ILC subpopulations were also analyzed by RNA sequencing and qPCR. Results: Alternaria exposure led to accumulation of all ILC populations regardless of ST2 or CD127 expression. Nearly half of the GATA-3+, IL-5+, and IL-13+ ILCs were “unconventional” as they were either single or double negative for ST2/CD127. Further, these populations upregulated CD25, KLRG1, and ICOS after Alternaria challenge. Some activated unconventional IL-5+ ILC2s also produced IFNγ and IL-17A. In addition to shared ILC2 transcripts (Gata3, Il5, Il13) in all populations, RNA-seq further identified novel transcripts enriched in each subset. Finally, transcripts from all populations that correlated best with IL-5 and IL-13 production included Tnfrsf18, Ffar2, and Pde4b. Conclusions: Unconventional ST2- and CD127-negative mouse lung ILC2 populations are induced by Alternaria. Thus, commonly used lung ILC2 identification methods based on ST2 and CD127 do not accurately account for the total ILC2 burden and may exclude nearly half of these cells.

2019-08-22 | GSE136156 | GEO

RNA-Seq of Group 2 innate lymphoid cells (ILC2) from lung and lymph node

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RNA-Seq of Group 2 innate lymphoid cells (ILC2) from uterine tissue (Virgin, E9.5, E18.5)

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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

Core Binding Factor β Is Required For Group-2 Innate Lymphoid Cell Activation

Project description:Group-2 innate lymphoid cells (ILC2) are tissue-resident, long-lived innate effector cells implicated in allergy and asthma. Upon activation, mature ILC2 rapidly secret large amounts of type-2 cytokines and other effector molecules. The molecular pathways that drive ILC2 activation are not well understood. Here we report that the transcriptional controller Core-binding factor β (CBFβ) is required for ILC2 activation. Deletion or inhibition of CBFβ did not impair the maintenance of ILC2 at homeostasis, but abolished ILC2 activation during allergic airway inflammation. Treatment with CBFβ inhibitors prevented ILC2-mediated airway hyperresponsiveness in a mouse model of acute Alternaria allergen inhalation. CBFβ promoted expression of key ILC2 genes at both transcriptional and translational levels. CBF transcriptional complex directly bound to Il13 and Vegfa promoters and enhancers, and controlled gene transcription. CBFβ further promoted ribosome biogenesis and enhanced gene translation in activated ILC2. Together, these data establish an essential role for CBFβ in ILC2 activation.

2019-01-23 | GSE116062 | GEO

ILC2-intrinsic IL-33 promotes ILC2 activation and exacerbates allergic lung 1 inflammation

Project description:Mass spectrometry-based proteomics serves as an invaluable tool for pinpointing critical biomarkers and elucidating cellular functions and regulatory pathways. However, the proteomic changes in ILC2s during activation remain unexplored. To characterize the dynamic proteomic profiles of lung-resident ILC2s under physiological and inflammatory conditions, we performed high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS) to systematically compare the molecular signatures of FACS-purified pulmonary ILC2 populations (Live CD45+CD90.2+Lineage- ST2+) isolated from two experimental groups: 1) steady-state control mice and 2) papain-challenged mice exhibiting acute airway inflammation (Fig. 1a and Supplementary Fig. 1a). Papain-induced lung inflammation was chosen because papain is a classical protease allergen triggering the release of pro-inflammatory factors including IL-33 to develop ILC2-derived lung inflammation.

2026-05-16 | PXD078462 |

Bulk RNA-Seq of lung Type 2 Innate Lymphoid cells (ILC2) in response to Alternaria alternata

Project description:Bulk RNA-Seq of lung Type 2 Innate Lymphoid cells (ILC2) in response to Alternaria alternata

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Unconventional ST2- and CD127-negative lung ILC2 populations are induced by Alternaria

Project description:Unconventional ST2- and CD127-negative lung ILC2 populations are induced by Alternaria

| PRJNA561402 | ENA

Transcription factor Bcl11b controls identity and function of mature innate lymphoid cells type II

Project description:Type-2 innate lymphoid cells (ILC2s) promote anti-helminth responses and contribute to allergies. Though Bcl11b has been previously considered a T-lineage identity transcription factor (TF) that restrains the innate-cell genetic programs, we report here that Bcl11b is highly expressed in mature ILC2s and acts upstream of the key ILC2 TFs Gfi1, Gata-3, and of IL-33 receptor IL1rl1 (T1ST2). Additionally, Bcl11b-/- ILC2s de-repressed Rorγt, Ahr and IL-23 receptor, normally expressed in type-3 ILCs (ILC3s). Consequently, Bcl11b-/- ILC2s lost ILC2 functions and gained ILC3 functions, expanding in response to the protease allergen papain, however producing IL-17 and IL-22, and not IL-5 and IL-13, causing lung neutrophilia rather than eosinophilia, and diminished mucus production. Our results broaden Bcl11b's role from a T-cell only TF, and establishes that Bcl11b sustains mature ILC2 genetic and functional programs and lineage fidelity through positive regulation of essential ILC2 TFs and negative regulation of pivotal ILC3 TFs. RNA-seq analysis on sorted ILC2s from the mLNs of Bcl11bF/F Cre-ERT2 and wildtype mice at steady state following tamoxifen mediated deletion of Bcl11b

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