ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Collaborative interactions between type 2 innate lymphoid cells and antigen-specific CD4+ Th2 cells exacerbate murine allergic airway diseases with prominent eosinophilia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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.
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Who cites it
32 citing papers in PubMed, 54 citations in OpenAlex.
- Trogocytosis and Allergy.Cells · 2026Review
- Prospects for developing allergen-depleted food crops.The plant genome · 2023Review
- Retinoic Acid-Related Orphan Receptor α Is Required for Generation of Th2 Cells in Type 2 Pulmonary Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Differential and cooperative effects of IL-25 and IL-33 on T helper cells contribute to cryptococcal virulence and brain infection.Scientific reports · 2023Article
- Class switching is differentially regulated in RBC alloimmunization and vaccination.Transfusion · 2023Article
- Adenosine restrains ILC2-driven allergic airway inflammation via A2A receptor.Mucosal immunology · 2022Article
- Crosstalk between ILC2s and Th2 CD4Journal of immunology research · 2022Review
- Physiological Convergence and Antagonism Between GR and PPARγ in Inflammation and Metabolism.Advances in experimental medicine and biology · 2022Review
- A Potential Role of Group 2 Innate Lymphoid Cells in Eosinophilic Chronic Rhinosinusitis With Nasal Polyps.Allergy, asthma & immunology research · 2021Review
- PPARγ enhances ILC2 function during allergic airway inflammation via transcription regulation of ST2.Mucosal immunology · 2021Article
- PD-1 expression affects cytokine production by ILC2 and is influenced by peroxisome proliferator-activated receptor-γ.Immunity, inflammation and disease · 2020Article
- Cell-surface molecule-mediated cell-cell interactions in the regulation of ILC2-driven allergic inflammation.Cellular and molecular life sciences : CMLS · 2019Review
- IL-25 Orchestrates Activation of Th Cells via Conventional Dendritic Cells in Tissue to Exacerbate Chronic House Dust Mite-Induced Asthma Pathology.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Th9 Cells in Allergic Disease.Current allergy and asthma reports · 2019Review
- Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses.Cellular & molecular immunology · 2019Review
- Innate Lymphoid Cells in Helminth Infections-Obligatory or Accessory?Frontiers in immunology · 2019Review
- Type 2 innate lymphoid cells in the induction and resolution of tissue inflammation.Immunological reviews · 2018Review
- ICAM-1 controls development and function of ILC2.The Journal of experimental medicine · 2018Article
- Interleukin-33 drives hepatic fibrosis through activation of hepatic stellate cells.Cellular & molecular immunology · 2018Article
- Guards at the gate: physiological and pathological roles of tissue-resident innate lymphoid cells in the lung.Protein & cell · 2017Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Type-2 innate lymphoid cells (ILC2s) and the acquired CD4(+) Th2 and Th17 cells contribute to the pathogenesis of experimental asthma; however, their roles in Ag-driven exacerbation of chronic murine allergic airway diseases remain elusive. In this study, we report that repeated intranasal rechallenges with only OVA Ag were sufficient to trigger airway hyperresponsiveness, prominent eosinophilic inflammation, and significantly increased serum OVA-specific IgG1 and IgE in rested mice that previously developed murine allergic airway diseases. The recall response to repeated OVA inoculation preferentially triggered a further increase of lung OVA-specific CD4(+) Th2 cells, whereas CD4(+) Th17 and ILC2 cell numbers remained constant. Furthermore, the acquired CD4(+) Th17 cells in Stat6(-/-)/IL-17-GFP mice, or innate ILC2s in CD4(+) T cell-ablated mice, failed to mount an allergic recall response to OVA Ag. After repeated OVA rechallenge or CD4(+) T cell ablation, the increase or loss of CD4(+) Th2 cells resulted in an enhanced or reduced IL-13 production by lung ILC2s in response to IL-25 and IL-33 stimulation, respectively. In return, ILC2s enhanced Ag-mediated proliferation of cocultured CD4(+) Th2 cells and their cytokine production, and promoted eosinophilic airway inflammation and goblet cell hyperplasia driven by adoptively transferred Ag-specific CD4(+) Th2 cells. Thus, these results suggest that an allergic recall response to recurring Ag exposures preferentially triggers an increase of Ag-specific CD4(+) Th2 cells, which facilitates the collaborative interactions between acquired CD4(+) Th2 cells and innate ILC2s to drive the exacerbation of a murine allergic airway diseases with an eosinophilic phenotype.
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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.