ArticleThe Journal of experimental medicine2023
TIGIT mediates activation-induced cell death of ILC2s during chronic airway allergy.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Heterogeneity and clinical relevance of group 2 innate lymphoid cells subsets in nasal polyps.The Journal of allergy and clinical immunology · 2026Article
- Review
- Engineered Neuromedin U Promotes Type 2 Innate Immunity and Renoprotection in Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
- Cellular Cosmetics: How Innate Lymphoid Cells Can Recontour the Tumour Microenvironment.European journal of immunology · 2025Review
- Update on type 2 immunity.The Journal of allergy and clinical immunology · 2025Review
- Multiple Myeloma Cells Shift the Fate of Cytolytic ILC2s Towards TIGIT-Mediated Cell Death.Cancers · 2025Article
- Unraveling resistance to immune checkpoint inhibitors in HNSCC: from mechanisms to combination therapies.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Dysfunction of type 1 and type 2 immune cells: a lesson from exhausted-like ILC2s and their activation-induced cell death.International immunology · 2024Review
- Acute Eosinophilic Pneumonia Induced by Immune Checkpoint Inhibitor and Anti-TIGIT Therapy.The American journal of case reports · 2024Article
- Review
- Mutant KRAS-activated circATXN7 fosters tumor immunoescape by sensitizing tumor-specific T cells to activation-induced cell death.Nature communications · 2024Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While group-2 innate lymphoid cells (ILC2s) are highly proliferative in allergic inflammation, the removal of overactivated ILC2s in allergic diseases has not been investigated. We previously showed that chronic airway allergy induces "exhausted-like" dysfunctional ILC2s expressing T cell immunoreceptor with Ig and ITIM domains (TIGIT). However, the physiological relevance of these cells in chronic allergy remains elusive. To precisely identify and monitor TIGIT+ ILC2s, we generated TIGIT lineage tracer mice. Chronic allergy stably induced TIGIT+ ILC2s, which were highly activated, apoptotic, and were quickly removed from sites of chronic allergy. Transcripts from coding genes were globally suppressed in the cells, possibly due to reduced chromatin accessibility. Cell death in TIGIT+ ILC2s was enhanced by interactions with CD155 expressed on macrophages, whereas genetic ablation of Tigit or blockade by anti-TIGIT antagonistic antibodies promoted ILC2 survival, thereby deteriorating chronic allergic inflammation. Our work demonstrates that TIGIT shifts the fate of ILC2s toward activation-induced cell death, which could present a new therapeutic target for chronic allergies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.