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Blocking CD226 regulates ILC2 effector function and alleviates airway hyperreactivity

GSE264060 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2024/04/16 Platform GPL19057
Summary
Type 2 innate lymphoid cells (ILC2s) play a pivotal role in type 2 asthma. CD226 is a costimulatory molecule involved in various inflammatory diseases. Here, we aimed to investigate CD226 expression and function within human and mouse ILC2s, and to assess the impact of targeting CD226 on ILC2-mediated airway hyperreactivity (AHR). Our findings demonstrated an inducible expression of CD226 in activated ILC2s, enhancing their cytokine secretion and effector functions. Blocking CD226 ameliorates ILC2-dependent AHR in IL-33 and Alternaria Alternata-induced models. Interestingly, CD226 is expressed and inducible in human ILC2s, and its blocking reduces cytokine production. Finally, we showed that peripheral ILC2s in asthmatic patients exhibited elevated CD226 expression compared to healthy controls.Our findings underscore the potential of CD226 as a novel therapeutic target in ILC2s, presenting a promising avenue for ameliorating AHR and allergic asthma.
Published in
Blocking CD226 regulates type 2 innate lymphoid cell effector function and alleviates airway hyperreactivity
Sakano Y, Sakano K, Hurrell BP et al. · The Journal of allergy and clinical immunology 2024 · PMID 38244725 · doi:10.1016/j.jaci.2024.01.003
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Also filed as BioProject PRJNA1100903 and SRA study SRP502005. Searching any of these in the dataset finder brings you back here.

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