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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
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RAG suppresses group 2 innate lymphoid cells.
Aaron M Ver Heul1, Madison Mack2, Lydia Zamidar3,4,5,6
1Division of Allergy and Immunology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63130, USA.
Biorxiv : the Preprint Server for Biology
|May 7, 2024
Summary
Recombinase Activating Gene (RAG) suppresses innate lymphoid cells (ILCs), revealing a new role in type 2 immunity. RAG deficiency in mice leads to expanded ILC2s and increased inflammation in atopic dermatitis models.
Area of Science:
- Immunology
- Molecular Biology
Background:
- Adaptive immunity relies on antigen specificity mediated by V(D)J recombination, involving Recombinase Activating Gene (RAG) endonucleases.
- Group 2 innate lymphoid cells (ILC2s) contribute to type 2 immune responses, but their regulation by RAG is unknown.
Purpose of the Study:
- To investigate the role of RAG in the function of ILC2s, a key component of innate type 2 immunity.
Main Methods:
- Utilized RAG-deficient mice to study ILC2 populations and cytokine production.
- Performed cell-intrinsic analyses, independent of adaptive lymphocytes.
- Employed multiomic single-cell analyses on RAG1 lineage-traced cells.
Main Results:
- RAG deficiency led to expanded ILC2 populations and increased Interleukin-5 (IL-5) and Interleukin-13 (IL-13) production.
- RAG modulated ILC2 function in a cell-intrinsic manner.
- Identified transcriptional and epigenomic programs in ILC2s suppressed by RAG expression.
Conclusions:
- RAG plays a novel suppressive role in innate type 2 immunity by regulating ILC2 function.
- This finding expands our understanding of immune regulation beyond adaptive immunity.
