ReviewExperimental & molecular medicine2023
The modulation of pulmonary group 2 innate lymphoid cell function in asthma: from inflammatory mediators to environmental and metabolic factors.
Review in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 34 citations in OpenAlex.
- Mechanisms and therapeutic strategies of asthma: from bench to bedside.Signal transduction and targeted therapy · 2026Review
- Identifying predictor factors for asthma using machine learning: evidence from the English Longitudinal Study of Ageing.BMC public health · 2026Article
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Metabolic Reprogramming and ILC2 Plasticity in Obesity-related Asthma.Clinical reviews in allergy & immunology · 2026Review
- HuR Regulates GATA3-Driven Type 2 Inflammation in CD4bioRxiv : the preprint server for biology · 2026Article
- Review
- Acute stress alleviates type 2 lung inflammation by restricting ILC2s through corticosterone-glucocorticoid receptor signaling.Cellular & molecular immunology · 2026Article
- Review
- Tim-3 agonist restrains ILC2 function and attenuates airway hyperreactivity via NLK pathway.Nature communications · 2026Article
- The context-dependent role of group 2 innate lymphoid cells in lung diseases.Acta biochimica et biophysica Sinica · 2026Review
- Pulmonary neuroendocrine cells in pediatric asthma and bronchopulmonary dysplasia: neuroimmune-developmental mechanisms and translational implications.Frontiers in medicine · 2026Review
- Microbial sensing through the non-canonical inflammasome modulates airway type 2 immunity.Frontiers in immunology · 2026Article
- The Expanding Role of ILC2s in Allergic Airways Disease.Allergy · 2026Review
- CD36 in asthma: from a candidate immunometabolic checkpoint to genetic susceptibility.Frontiers in immunology · 2026Review
- The lung microbiome and asthma: from inflammatory phenotype differentiation to microbe-based immunomodulatory strategies.Frontiers in immunology · 2026Review
- Effect of Xuanfei Tongqiao acupuncture on nasal inflammation in rats with allergic rhinitis: modulation of long non-coding RNA growth arrest-specific transcript 5 methylation modification.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Biologic Therapies for Severe Asthma: Current Insights and Future Directions.Journal of clinical medicine · 2025Review
- Chronic Inflammation in Asthma: Looking Beyond the Th2 Cell.Immunological reviews · 2025Review
- Emerging Concepts in Cytokine Regulation of Airway Remodeling in Asthma.Immunological reviews · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A dysregulated type 2 immune response is one of the fundamental causes of allergic asthma. Although Th2 cells are undoubtedly central to the pathogenesis of allergic asthma, the discovery of group 2 innate lymphoid cells (ILC2s) has added another layer of complexity to the etiology of this chronic disease. Through their inherent innate type 2 responses, ILC2s not only contribute to the initiation of airway inflammation but also orchestrate the recruitment and activation of other members of innate and adaptive immunity, further amplifying the inflammatory response. Moreover, ILC2s exhibit substantial cytokine plasticity, as evidenced by their ability to produce type 1- or type 17-associated cytokines under appropriate conditions, underscoring their potential contribution to nonallergic, neutrophilic asthma. Thus, understanding the mechanisms of ILC2 functions is pertinent. In this review, we present an overview of the current knowledge on ILC2s in asthma and the regulatory factors that modulate lung ILC2 functions in various experimental mouse models of asthma and in humans.
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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.