ArticleCurrent trends in immunology2022
Modulating ILC2 function for treatment of type 2 airway diseases.
Article in Current trends in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 2 citations in OpenAlex.
- Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026Review
- Immune-inflammatory endotypes of chronic rhinosinusitis: from epithelial alarmins to personalized therapy.Frontiers in immunology · 2026Review
- Bibliometric analysis of T cells in allergic rhinitis.Heliyon · 2024Review
- ILC2-mediated immune crosstalk in chronic (vascular) inflammation.Frontiers in immunology · 2023Review
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
Type 2 airway diseases including chronic rhinosinusitis, allergic rhinitis, and asthma remain a major health concern. These disorders are largely characterized by an uncontrolled type 2 immune response with elevated cytokines of IL-4, IL-5 and IL-13, eosinophilic inflammation, goblet cell hyperplasia as well as tissue remodeling. In the last few decades, critical potential roles of innate lymphoid cells (ILCs) in type 2 human diseases have emerged. Unlike their lymphocyte counterpart T cells, ILCs lack antigen-specific receptors and are largely tissue resident. Specifically, group 2 innate lymphoid cells (ILC2s) respond to airway epithelium-derived alarmins (TSLP, IL-33) and secrete high levels of type 2 cytokines. ILC2 responses can bypass the activation of T cells as well as develop corticosteroid-resistance. Currently approved biologics targeting the alarmin thymic stromal lymphopoietin (TSLP) or the IL-4/IL-13 receptor may reduce ILC2 activation, though novel treatments of type 2 airway diseases remain needed. In this review, we briefly discuss the pathogenesis of ILC2-mediated airway diseases followed by their current and potential treatments.
Indexed as
Identifiers
37396395PMC10311961W4382918614What 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.