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Nr4a1 marks a distinctive ILC2 activation subset in the mouse inflammatory lung
Shasha Xu1, Yu Zhang1, Xingjie Liu1
1Department of Hematology, Tongji Hospital, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.
BMC Biology
|October 13, 2023
Summary
Group 2 innate lymphoid cells (ILC2s) are diverse, with a subset expressing Nr4a1. Programmed cell death protein-1 (PD-1) restrains ILC2 activation, and its absence promotes ILC2 expansion and differentiation.
Area of Science:
- Immunology
- Cell Biology
- Innate Immunity
Background:
- Group 2 innate lymphoid cells (ILC2s) are key producers of type 2 cytokines in the mouse lung.
- The molecular mechanisms governing ILC2 activation during inflammatory responses remain incompletely understood.
Purpose of the Study:
- To elucidate the heterogeneity of ILC2 subsets during acute lung inflammation.
- To investigate the role of programmed cell death protein-1 (PD-1) in regulating ILC2 activation and subset differentiation.
Main Methods:
- Single-cell transcriptomics
- Genetic reporters
- Gene knockouts in mouse models
Main Results:
- Identified four ILC2 subsets in the inflamed mouse lung: two non-activation and two activation subsets.
- Discovered a novel activation subset (Nr4a1+) expressing memory T cell signatures, proliferation, and wound healing markers.
- Demonstrated that PD-1 negatively regulates Nr4a1+ ILC2 activation and that PD-1 deficiency promotes ILC2 activation, differentiation, and expansion.
Conclusions:
- Activated ILC2s represent a heterogeneous population with distinct subset propensities.
- PD-1 plays a crucial role in modulating ILC2 activity, offering potential therapeutic targets for inflammatory diseases.
