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Related Concept Videos

Lymphoid Cells and Tissues01:18

Lymphoid Cells and Tissues

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Related Experiment Video

Updated: Mar 2, 2026

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
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Immune checkpoints on innate lymphoid cells.

Laura Chiossone1, Eric Vivier1

  • 1Centre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille, France; Service d'Immunologie, Hôpital de la Timone, Assistance Publique-Hôpitaux de Marseille, Marseille, France.

The Journal of Experimental Medicine
|May 19, 2017
PubMed
Summary

Programmed cell death protein 1 (PD-1) acts as a key inhibitor of group 2 innate lymphoid cells (ILC-2s). Blocking PD-1 enhances ILC-2 function and improves parasite infection clearance in mice.

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Area of Science:

  • Immunology
  • Innate Immunity
  • Cellular Regulation

Background:

  • Group 2 innate lymphoid cells (ILC-2s) are crucial for immune responses against helminth infections and allergic inflammation.
  • The precise regulatory mechanisms governing ILC-2 function remain incompletely understood.

Purpose of the Study:

  • To investigate the role of programmed cell death protein 1 (PD-1) in regulating ILC-2 activity.
  • To determine the impact of PD-1 signaling on ILC-2 proliferation, cytokine production, and in vivo function.

Main Methods:

  • Analysis of PD-1 expression on mouse and human ILC-2s.
  • In vitro studies involving PD-1 knockdown or blocking antibodies to assess effects on STAT5 phosphorylation, proliferation, and cytokine production.
  • In vivo experiments using anti-PD-1 antibodies in a helminth infection model.

Main Results:

  • PD-1 was identified as a critical intrinsic negative regulator of both mouse and human ILC-2s.
  • PD-1 signaling was shown to inhibit STAT5 phosphorylation, a key pathway for ILC-2 activation.
  • Inhibition of PD-1 signaling in vivo led to enhanced clearance of helminth worm infection in mice.

Conclusions:

  • PD-1 plays a significant role in suppressing ILC-2 function.
  • Targeting PD-1 represents a potential therapeutic strategy to boost ILC-2-mediated immunity against parasitic infections.