ReviewFrontiers in immunology2018
Social Networking of Group Two Innate Lymphoid Cells in Allergy and Asthma.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
45 citing papers in PubMed, 60 citations in OpenAlex.
- MyD88 mediates allergic airway inflammation by regulating ILC2s function through inducing the formation of P38/GATA3 complex.Respiratory research · 2026Article
- Tim-3 agonist restrains ILC2 function and attenuates airway hyperreactivity via NLK pathway.Nature communications · 2026Article
- Transcription Factor Blimp-1: A Central Regulator of Oxidative Stress and Metabolic Reprogramming in Chronic Inflammatory Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- SIRPα engagement regulates ILC2 effector function and alleviates airway hyperreactivity via modulating energy metabolism.Cellular & molecular immunology · 2024Article
- Piezo1 channels restrain ILC2s and regulate the development of airway hyperreactivity.The Journal of experimental medicine · 2024Article
- The Functional Role of Group 2 Innate Lymphoid Cells in Asthma.Biomolecules · 2023Review
- Programmed Cell Death in Asthma: Apoptosis, Autophagy, Pyroptosis, Ferroptosis, and Necroptosis.Journal of inflammation research · 2023Review
- Innate lymphoid cells in depression: Current status and perspectives.Biomarkers in neuropsychiatry · 2022Article
- Identification of the niche and mobilization mechanism for tissue-protective multipotential bone marrow ILC progenitors.Science advances · 2022Article
- Potential Therapeutic Skin Microbiomes SuppressingInternational journal of molecular sciences · 2022Article
- RNA-binding protein RBM3 intrinsically suppresses lung innate lymphoid cell activation and inflammation partially through CysLT1R.Nature communications · 2022Article
- Hypoxia induces adrenomedullin from lung epithelia, stimulating ILC2 inflammation and immunity.The Journal of experimental medicine · 2022Article
- Cannabinoid receptor 2 engagement promotes group 2 innate lymphoid cell expansion and enhances airway hyperreactivity.The Journal of allergy and clinical immunology · 2022Article
- Innate lymphocytes: Role in alcohol-induced immune dysfunction.Frontiers in immunology · 2022Review
- Toward a More Precise Solution to Asthma Therapy.American journal of respiratory cell and molecular biology · 2021Article
- CD52-targeted depletion by Alemtuzumab ameliorates allergic airway hyperreactivity and lung inflammation.Mucosal immunology · 2021Article
- New Treatments for Atopic Dermatitis Targeting Skin Barrier Repair via the Regulation of FLG Expression.Journal of clinical medicine · 2021Review
- CD200-CD200R immune checkpoint engagement regulates ILC2 effector function and ameliorates lung inflammation in asthma.Nature communications · 2021Article
- PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2.Mucosal immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Allergic diseases including asthma, chronic rhinosinusitis, and atopic dermatitis are common conditions worldwide. While type 2 immune responses induced by T-cells significantly cause allergic inflammation, the recently identified group two innate lymphoid cells (ILC2s) are emerging as critical players in the development of allergy. Upon allergen exposure, ILC2s are rapidly activated by cytokines released by epithelial cells. Activated ILC2s release various effector cytokines altogether contributing to the pathogenesis of allergy and can even cause inflammation in the absence of T-cells, as observed in asthma. Although the factors inducing ILC2 activation have been identified, evidence suggests that multiple factors can enhance or repress ILC2 proliferation, trafficking, or secretion of effector cytokines upon allergic inflammation. In this review, we discuss the recent findings that influence ILC2 activation and the resulting effects on the pathogenesis of allergy. A better understanding of how ILC2s are modulated will open the door to the development of new therapeutic strategies against allergic diseases.
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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.