ReviewAllergy2026
The Expanding Role of ILC2s in Allergic Airways Disease.
Review in Allergy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Subcutaneous immunotherapy-induced IgG1 suppresses allergic airway inflammation through FcγRIIb-mediated inhibition of group 2 innate lymphoid cell proliferation.The World Allergy Organization journal · 2026Article
- Baicalein mitigates epithelial barrier impairment and microbiota dysbiosis in allergic asthmatic mice via the gut‑lung axis.Chinese medicine · 2026Article
- CD36 in asthma: from a candidate immunometabolic checkpoint to genetic susceptibility.Frontiers in immunology · 2026Review
- Melatonin suppresses ILC2-driven airway hyperreactivity via glutathione-dependent metabolic reprogramming.Frontiers in immunology · 2026Article
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.
Funding
Abstract
Group 2 innate lymphoid cells (ILC2s) play a pivotal role in the initiation and propagation of allergic airways disease. These cells, first discovered 15 years ago, respond to a range of stimuli in a non-antigen-dependent manner. ILC2s produce copious amounts of cytokines including IL-5 and IL-13, which are critical in the pathogenesis of allergic asthma. While allergic airways diseases have long been considered T-helper 2 cell-driven diseases, ILC2s are capable of inducing allergic-type pathologies in mice even in the absence of the adaptive immune system. The role of ILC2s in driving the pathology of allergic airways disease remains an expanding field of knowledge that may unlock novel therapeutic approaches in the management of asthma, a disease that affects up to 300 million people worldwide. In this review, we survey current knowledge of ILC2 immunobiology and present an overview of ILC2 phenotyping, concurrent with insights into ILC2 plasticity, and an exploration of the roles of costimulatory molecules, neuroendocrine signals, and diet-derived nutrients in modulating ILC2 activity.
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Identifiers
What OpenQuestion holds
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.