Insights into Group 2 Innate Lymphoid Cells in Human Airway Disease
Open accessAbstract
Recent discoveries have led to the identification of a novel group of immune cells, the innate lymphoid cells (ILCs). The members of this group are divided into three subpopulations: ILC1s, ILC2s, and ILC3s. ILC2s produce Th2 cytokines, IL-4, IL-5, and IL-13, upon activation by epithelial cell-derived cytokines, lipid mediators (cysteinyl leukotrienes and prostaglandin D2), and TNF family member TL1A and promote structural and immune cell responses in the airways after antigen exposure. In addition, ILC2 function is also influenced by inducible T cell costimulator (ICOS)/ICOS-ligand (ICOS-L) interactions via direct contact between immune cells. The most common airway antigens are allergens and viruses which are highly linked to the induction of airway diseases with underlying type 2 inflammation including asthma and allergic rhinitis. Based on recent findings linking ILC2s and airway Th2 responses, there is intensive investigation into the role of ILC2s in human disease with the hope of a better understanding of the pathophysiology and the discovery of novel potential therapeutic targets. This review summarizes the recent advances made in elucidating ILC2 involvement in human Th2 airway disease.
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Upon exposure to environmental antigens including viruses and allergens, airway epithelial cells rapidly release IL-25, IL-33, and TSLP, which directly activate ILC2s that then produce IL-5 and IL-13.
“Upon exposure to environmental antigens, including viruses and allergens, airway epithelial cells rapidly release the cytokines IL-25, IL-33, and TSLP which directly activate ILC2s that then produce the prototypical type 2 cytokines IL-5 and IL-13.331”
From International Consensus Statement on Allergy and Rhinology: Allergic Rhinitis (2018) · cites this paper as [331]
The “Sources of ILC2 Activation” section identifies IL-25, IL-33, and TSLP as epithelial-cell-derived activators of ILC2s and reports that activated ILC2s produce IL-5 and IL-13. The sections on TSLP and on allergen- and virus-induced responses connect these pathways to allergens and infections. The copy does not establish that epithelial cells rapidly release all three cytokines upon either type of exposure; no page numbers are available in the indexed passages. (LLM, conf=0.84)
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References 125 · Cited by 77
Research works printed but not linked: 1
- [111]Christianson CA Goplen NP Zafar I Irvin C Good JT Jr Rollins DR Persistence of asthma requires multiple feedback circuits involving type 2 innate lymphoid cells and IL-33 J Allergy Clin Immunol 2015 136 59 68.e14 25617223 PMC4494983
- Authors
- Karta, M. R., Broide, D. H., & Doherty, T. A.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Doherty, Taylor A.
- Venue
- Current Allergy and Asthma Reports
- Published
- 2016-01
- Volume
- 16
- Issue
- 1
- Pages
- 8-8
- ISSN
- 1529-7322 (ISSN-L)
- 1534-6315
- PMC
- PMC5026503
- OpenAlex
- W2229487052
- Cited by
- 77
- References
- 125
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 5 · 2023: 6 · 2022: 5 · 2021: 7 · 2020: 8 · 2019: 12 · 2018: 11 · 2017: 16 · 2016: 4
- FWCI
- 1.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Allergy and Asthma Reports (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (R01 AI114585, AI 107779, AI 38425, AI 70535, T32 AI007469)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Keywords
- ILC2, type 2 inflammation, airway disease, asthma, allergic rhinitis, cysteinyl leukotrienes, prostaglandin D2, TL1A, airway epithelium, therapeutic target
- MeSH terms
- Allergens, Asthma, Humans, Immunity, Innate, Lymphocytes, Respiratory System, Cytokines, Rhinitis, Allergic
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