ArticleCellular & molecular immunology2019
Kinetics of the accumulation of group 2 innate lymphoid cells in IL-33-induced and IL-25-induced murine models of asthma: a potential role for the chemokine CXCL16.
Article in Cellular & molecular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- Interleukin-4-producing type 2 innate lymphoid cells in the lymph node promote proallergic Tfh13 cell differentiation.Immunity · 2026Article
- Intestinal host-microbe interactions fuel pulmonary inflammation in cigarette smoke exposed mice.Gut microbes · 2025Article
- CXCL16 knockout inhibit asthma airway inflammation by suppressing H2-DM molecular mediated antigen presentation.Cell death discovery · 2025Article
- Application of Biologics in the Treatment of Asthma in the Past Two Decades: A Bibliometric Analysis and Beyond.Journal of asthma and allergy · 2025Review
- Unspoken words: decoding the dialog between type 2 innate lymphoid cells and T cells.Frontiers in immunology · 2025Review
- Immunological factors, important players in the development of asthma.BMC immunology · 2024Review
- Airways epithelial exposure to Streptococcus pneumoniae in the presence of the alarmin IL-33 induces a novel subset of pro-inflammatory ILC2s promoting a mixed inflammatory response.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- SLAM-family receptors promote resolution of ILC2-mediated inflammation.Nature communications · 2024Article
- LSD1 drives intestinal epithelial maturation and controls small intestinal immune cell composition independent of microbiota in a murine model.Nature communications · 2024Article
- Dietary Fiber-Derived Microbial Butyrate Suppresses ILC2-Dependent Airway Inflammation in COPD.Mediators of inflammation · 2024Article
- Immunotherapeutic implications on targeting the cytokines produced in rhinovirus-induced immunoreactions.Frontiers in allergy · 2024Review
- Unraveling the Role of Epithelial Cells in the Development of Chronic Rhinosinusitis.International journal of molecular sciences · 2023Review
- Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells.Cardiovascular research · 2023Article
- Single-cell landscape dissecting the transcription and heterogeneity of innate lymphoid cells in ischemic heart.Frontiers in immunology · 2023Article
- The absence of IL-9 reduces allergic airway inflammation by reducing ILC2, Th2 and mast cells in murine model of asthma.BMC pulmonary medicine · 2022Article
- Akt isoforms in the immune system.Frontiers in immunology · 2022Review
- Plasticity of Innate Lymphoid Cells in Cancer.Frontiers in immunology · 2022Review
- The potential roles of interleukin-25 in infectious diseases.Frontiers in immunology · 2022Review
- Review
- Cycloastragenol alleviates airway inflammation in asthmatic mice by inhibiting autophagy.Molecular medicine reports · 2021Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ILC2s are implicated in asthma pathogenesis, but little is known about the mechanisms underlying their accumulation in airways. We investigated the time course of ILC2 accumulation in different tissues in murine models of asthma induced by a serial per-nasal challenge with ovalbumin (OVA), house dust mice (HDM), IL-25 and IL-33 and explored the potential roles of ILC2-attracting chemokines in this phenomenon. Flow cytometry was used to enumerate ILC2s at various time points. The effects of cytokines and chemokines on ILC2 migration were measured in vitro using a chemotaxis assay and in vivo using small animal imaging. Compared with saline and OVA challenge, both IL-25 and IL-33 challenge alone induced significant accumulation of ILC2s in the mediastinal lymph nodes, lung tissue and bronchoalveolar lavage fluid of challenged animals, but with a distinct potency and kinetics. In vitro, IL-33 and CXCL16, but not IL-25 or CCL25, directly induced ILC2 migration. Small animal in vivo imaging further confirmed that a single intranasal provocation with IL-33 or CXCL16 was sufficient to induce the accumulation of ILC2s in the lungs following injection via the tail vein. Moreover, IL-33-induced ILC2 migration involved the activation of ERK1/2, p38, Akt, JNK and NF-κB, while CXCL16-induced ILC2 migration involved the activation of ERK1/2, p38 and Akt. These data support the hypothesis that epithelium-derived IL-25 and IL-33 induce lung accumulation of ILC2s, while IL-33 exerts a direct chemotactic effect in this process. Although ILC2s express the chemokine receptors CXCR6 and CCR9, only CXCL16, the ligand of CXCR6, exhibits a direct chemoattractant effect.
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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.