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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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A CCL1/CCR8-dependent feed-forward mechanism drives ILC2 functions in type 2-mediated inflammation
Lisa Knipfer1, Anja Schulz-Kuhnt1, Markus Kindermann1
1Department of Medicine 1, University Hospital Center, Friedrich-Alexander University, Erlangen-Nuremberg, Germany.
The Journal of Experimental Medicine
|September 21, 2019
Summary
Group 2 innate lymphoid cells (ILC2s) play key roles in type 2 inflammation. This study reveals that CCL1 signaling to ILC2s promotes their proliferation and enhances protection against helminth infections.
Area of Science:
- Immunology
- Cell Biology
Background:
- Group 2 innate lymphoid cells (ILC2s) are crucial in type 2 inflammatory diseases.
- Understanding ILC2 tissue tropism and self-renewal regulation during inflammation is incomplete.
Purpose of the Study:
- To investigate the role of CC-chemokine receptor 8 (CCR8) in ILC2 biological functions.
- To elucidate the molecular mechanisms regulating ILC2 proliferation and function in type 2 responses.
Main Methods:
- In vitro and in vivo experiments were conducted.
- Analysis of CCR8 and its ligand CCL1 in mouse and human ILC2s.
- Assessment of ILC2 proliferation and helminth infection protection.
Main Results:
- CCR8 is less critical for ILC2 migration compared to CCR4.
- Activated mouse and human ILC2s are major producers of the CCR8 ligand CCL1.
- CCL1 signaling to ILC2s enhances their proliferation and protective capacity against helminth infections.
Conclusions:
- A novel CCR8-dependent mechanism regulates ILC2s during type 2 immune responses.
- CCL1-CCR8 axis is identified as a key regulator of ILC2 self-renewal and function.
- This finding offers insights into ILC2-mediated inflammatory diseases and helminth immunity.
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