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Related Experiment Video

Updated: Jul 5, 2025

Isolation of Group 2 Innate Lymphoid Cells from Mouse Nasal Mucosa to Detect the Expression of CD226
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Blocking CD226 regulates type 2 innate lymphoid cell effector function and alleviates airway hyperreactivity.

Yoshihiro Sakano1, Kei Sakano1, Benjamin P Hurrell1

  • 1Department of Molecular Microbiology and Immunology, Keck School of Medicine of the University of Southern California, Los Angeles, Calif.

The Journal of Allergy and Clinical Immunology
|January 20, 2024
PubMed
Summary

Blocking CD226 reduces airway hyperreactivity by targeting type 2 innate lymphoid cells (ILC2s). This molecule is upregulated in asthma, making it a potential therapeutic target for allergic asthma.

Keywords:
CD226Type 2 innate lymphoid cellsairway hyperreactivityallergyasthma

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Area of Science:

  • Immunology
  • Cell Biology
  • Allergy Research

Background:

  • Type 2 innate lymphoid cells (ILC2s) are key players in type 2 asthma.
  • CD226 is a costimulatory molecule implicated in inflammatory conditions.

Purpose of the Study:

  • Investigate CD226 expression and function in mouse and human ILC2s.
  • Assess the therapeutic potential of targeting CD226 for ILC2-mediated airway hyperreactivity (AHR).

Main Methods:

  • Administered IL-33 to mice, followed by anti-CD226 antibody treatment.
  • Analyzed pulmonary ILC2s using RNA sequencing and flow cytometry.
  • Evaluated CD226 effects on AHR and inflammation in mouse models and human samples.

Main Results:

  • CD226 expression is inducible in activated ILC2s, enhancing cytokine secretion and effector functions.
  • CD226 modulates intracellular metabolism and signaling pathways (PI3K/AKT, MAPK).
  • Blocking CD226 ameliorates ILC2-dependent AHR and reduces cytokine production in human ILC2s.
  • Elevated CD226 expression observed in ILC2s from asthmatic patients.

Conclusions:

  • CD226 is a promising therapeutic target for allergic asthma.
  • Targeting CD226 offers a potential strategy to ameliorate AHR.