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Updated: Mar 19, 2026

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
Published on: May 10, 2022
G9a regulates group 2 innate lymphoid cell development by repressing the group 3 innate lymphoid cell program
Frann Antignano1, Mitchell Braam2, Michael R Hughes2
1The Biomedical Research Centre, University of British Columbia, Vancouver, British Columbia V6T 1Z3, Canada colby.zaph@monash.edu frann@brc.ubc.ca.
The study reveals the enzyme G9a is crucial for the development and function of group 2 innate lymphoid cells (ILC2s). Its absence impairs ILC2s, preventing allergic lung inflammation by repressing ILC3 genes.
Area of Science:
- Immunology
- Epigenetics
- Cell Biology
Background:
- Innate lymphoid cells (ILCs) are key immune regulators in health and disease.
- Epigenetic mechanisms governing ILC biology remain largely unexplored.
- Understanding ILC regulation is vital for immune-related therapies.
Purpose of the Study:
- To investigate the role of epigenetic mechanisms in ILC development and function.
- To identify specific epigenetic regulators involved in ILC biology.
- To elucidate the function of lysine methyltransferase G9a in ILC2s.
Main Methods:
- Hematopoietic cell-specific deletion of G9a in mice (Vav.G9a(-/-)).
- Analysis of ILC2 populations in peripheral sites and bone marrow.
- Genome-wide expression analysis and histone modification profiling (H3K9me2).
Main Results:
- Vav.G9a(-/-) mice showed significantly reduced ILC2 numbers and impaired development.
- These mice were resistant to allergic lung inflammation.
- G9a absence led to increased expression of ILC3-associated genes in ILC2s due to reduced H3K9me2 repression.
Conclusions:
- G9a is essential for the proper development and function of ILC2s.
- G9a-mediated epigenetic repression of ILC3-specific genes is critical for ILC2 development.
- This study identifies a novel epigenetic regulatory mechanism in ILC biology.
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