ArticlePloS one2017
NKT cells contribute to basal IL-4 production but are not required to induce experimental asthma.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Natural killer T cells in allergic asthma: implications for the development of novel immunotherapeutical strategies.Frontiers in immunology · 2024Review
- Review
- Invariant natural killer T cells balance B cell immunity.Immunological reviews · 2021Review
- New Insights into Asthma Inflammation: Focus on iNKT, MAIT, and γδT Cells.Clinical reviews in allergy & immunology · 2020Review
- An Update on the Pathogenesis of Cutaneous Lupus Erythematosus and Its Role in Clinical Practice.Current rheumatology reports · 2020Review
- IL-4Rα expression by airway epithelium and smooth muscle accounts for nearly all airway hyperresponsiveness in murine allergic airway disease.Mucosal immunology · 2020Article
- The role of invariant T cells in inflammation of the skin and airways.Seminars in immunopathology · 2019Review
- Role of Natural Killer T (NKT) Cells in Type II Diabetes-Induced Vascular Injuries.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Tissue-specific functions of invariant natural killer T cells.Nature reviews. Immunology · 2018Review
- Lipid-Reactive T Cells in Immunological Disorders of the Lung.Frontiers in immunology · 2018Review
- Role of CD1d- and MR1-Restricted T Cells in Asthma.Frontiers in immunology · 2018Review
- Role of inflammatory cells in pathophysiology and management of diabetic retinopathy.Survey of ophthalmologyReview
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
CD1d-deficiency results in a selective deletion of NKT cells in mice that is reported to prevent murine allergic airway disease (AAD). Because we find 2-3 fold lower basal IL-4 production in CD1d- mice than in wild-type (WT) mice, we hypothesized that the contribution made by NKT cells to AAD would depend on the strength of the stimulus used to induce the disease. Consequently, we compared CD1d-deficient mice to WT mice in the development of AAD, using several models of disease induction that differed in the type and dose of allergen, the site of sensitization and the duration of immunization. Surprisingly we found equivalent allergic inflammation and airway disease in WT and CD1d- mice in all models investigated. Consistent with this, NKT cells constituted only ~2% of CD4+ T cells in the lungs of mice with AAD, and IL-4-transcribing NKT cells did not expand with disease induction. Concerned that the congenital absence of NKT cells might have caused a compensatory shift within the immune response, we administered an anti-CD1d monoclonal Ab (mAb) to block NKT function before airway treatments, before or after systemic sensitization to antigen. Such Ab treatment did not affect disease severity. We suggest that the differences reported in the literature regarding the significance of NKT cells in the induction of allergic airway disease may have less to do with the methods used to study the disease and more to do with the animals themselves and/or the facilities used to house them.
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Registered trials
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