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Maternal Asthma During Pregnancy Imprints Fetal Lung Group 2 Innate Lymphoid Cells [snRNA-Seq]

ABSTRACT: We investigated the effects on the lungs during fetal in the offspring of asthmatic mothers. Lung ILC2 of offspring of asthmatic mothers altered phenotypically during fetal life.

ORGANISM(S): Mus musculus

PROVIDER: GSE262715 | GEO | 2024/12/01

REPOSITORIES: GEO

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Maternal Asthma During Pregnancy Imprints Histone Modification of Lung Group 2 Innate Lymphoid Cells

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Maternal Asthma During Pregnancy Imprints Fetal Lung Group 2 Innate Lymphoid Cells and Enhances Their Function in Adulthood [scATAC-Seq]

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Maternal Asthma During Pregnancy Imprints Fetal Lung Group 2 Innate Lymphoid Cells [snRNA-Seq]

Project description:Maternal Asthma During Pregnancy Imprints Fetal Lung Group 2 Innate Lymphoid Cells [snRNA-Seq]

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Maternal Stress During Pregnancy Imprints Fetal Lung Group 2 Innate Lymphoid Cells

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Ang II enhances group 2 innate lymphoid cell responses via AT1a during airway inflammation

Project description:Group 2 innate lymphoid cells (ILC2s) have emerged as critical mediators in driving allergic airway inflammation. Here, we identified angiotensin (Ang) II as a positive regulator of ILC2s. ILC2s expressed higher levels of the Ang II receptor AT1a, and colocalized with lung epithelial cells expressing angiotensinogen. Administration of Ang II significantly enhanced ILC2 responses both in vivo and in vitro, which were almost completely abrogated in AT1a-deficient mice. Deletion of AT1a or pharmacological inhibition of the Ang II - AT1 axis resulted in a remarkable remission of airway inflammation. The regulation of ILC2s by Ang II was cell-intrinsic and dependent on interleukin (IL)-33, and was associated with marked changes in transcriptional profiling and upregulation of ERK1/2 phosphorylation. Furthermore, higher levels of plasma Ang II correlated positively with the abundance of circulating ILC2s as well as disease severity in asthmatic patients. These observations reveal a critical role for Ang II in regulating ILC2 responses and airway inflammation.

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

Project description:Group 2 innate lymphoid cells (ILC2) promote the production of a type-2 immunological environment in the uterus and have tissue-specific gene signatures that change with pregnancy.

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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.

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Non-redundant functions of group 2 innate lymphoid cells

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