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Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226

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ILC2s regulate adaptive Th2 cell functions via PD-L1 checkpoint control.

Christian Schwartz^1,2, Adnan R Khan^1,2, Achilleas Floudas^1,2

¹Trinity Biomedical Sciences Institute, School of Medicine, Trinity College Dublin, Dublin, Ireland.

The Journal of Experimental Medicine

|July 28, 2017

Summary

This summary is machine-generated.

Group 2 innate lymphoid cells (ILC2s) express PD-L1, enhancing T helper 2 (Th2) cell responses. This PD-L1 checkpoint on ILC2s promotes type 2 immunity, impacting inflammation treatments.

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Area of Science:

Immunology
Cell Biology

Background:

Group 2 innate lymphoid cells (ILC2s) initiate type 2 immune responses.
Adaptive T helper 2 (Th2) immunity is crucial for type 2 responses.

Purpose of the Study:

To investigate the role of PD-L1 expression on ILC2s in type 2 immune responses.
To elucidate the mechanism by which ILC2-expressed PD-L1 influences Th2 cell differentiation and function.

Main Methods:

Analysis of PD-L1 expression on ILC2s during type 2 pulmonary responses.
In vitro and in vivo experiments assessing the impact of PD-L1:PD-1 interactions on T cell responses.
Conditional deletion of PD-L1 on ILC2s in a helminth infection model.

Main Results:

ILC2s dynamically express PD-L1 during type 2 immune responses.
PD-L1 on ILC2s enhances GATA3 expression and IL-13 production by Th2 cells.
Deletion of PD-L1 on ILC2s impairs Th2 polarization and delays parasite clearance.

Conclusions:

ILC2s utilize PD-L1 as an innate checkpoint to regulate adaptive Th2 responses.
PD-L1-mediated ILC2 function is critical for effective type 2 immunity.
This finding has implications for treating type 2 inflammatory diseases.