ArticleMucosal immunology2015
Trif-dependent induction of Th17 immunity by lung dendritic cells.
Article in Mucosal immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Effect of propolis on Th2 and Th17 cells: interplay with EtxB- and LPS-treated dendritic cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2023Article
- CD11bNature communications · 2021Article
- Tissue-Specific Contributions to Control of T Cell Immunity.ImmunoHorizons · 2021Article
- Toll-Like Receptor 3-TRIF Pathway Activation byInfection and immunity · 2019Article
- Pathogenic TThe Journal of allergy and clinical immunology · 2018Article
- Human iPSC-MSCs prevent steroid-resistant neutrophilic airway inflammation via modulating Th17 phenotypes.Stem cell research & therapy · 2018Article
- Oxidative stress and cellular pathways of asthma and inflammation: Therapeutic strategies and pharmacological targets.Pharmacology & therapeutics · 2018Review
- Asthma Biomarkers: Do They Bring Precision Medicine Closer to the Clinic?Allergy, asthma & immunology research · 2017Review
- The TLR4-TRIF pathway can protect against the development of experimental allergic asthma.Immunology · 2017Article
- Engaging the CD40-CD40L pathway augments T-helper cell responses and improves control of Mycobacterium tuberculosis infection.PLoS pathogens · 2017Article
- Cytokine regulation of lung Th17 response to airway immunization using LPS adjuvant.Mucosal immunology · 2017Article
- Review
- Advanced Role of Neutrophils in Common Respiratory Diseases.Journal of immunology research · 2017Review
- Leishmaniavirus-Dependent Metastatic Leishmaniasis Is Prevented by Blocking IL-17A.PLoS pathogens · 2016Article
- TRIF Deficiency does not Affect Severity of Ovalbumin-induced Airway Inflammation in Mice.Immune network · 2014Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Allergic asthma is thought to stem largely from maladaptive T helper 2 (Th2) responses to inhaled allergens, which in turn lead to airway eosinophilia and airway hyperresponsiveness (AHR). However, many individuals with asthma have airway inflammation that is predominantly neutrophilic and resistant to treatment with inhaled glucocorticoids. An improved understanding of the molecular basis of this form of asthma might lead to improved strategies for its treatment. Here, we identify novel roles of the adaptor protein, TRIF (TIR-domain-containing adapter-inducing interferon-β), in neutrophilic responses to inhaled allergens. In different mouse models of asthma, Trif-deficient animals had marked reductions in interleukin (IL)-17, airway neutrophils, and AHR compared with wild-type (WT) mice, whereas airway eosinophils were generally similar in these two strains. Compared with lung dendritic cells (DCs) from WT mice, lung DCs from Trif-deficient mice displayed impaired lipopolysaccharide (LPS)-induced migration to regional lymph nodes, lower levels of the costimulatory molecule, CD40, and produced smaller amounts of the T helper 17 (Th17)-promoting cytokines, IL-6, and IL-1β. When cultured with allergen-specific, naive T cells, Trif-deficient lung DCs stimulated robust Th2 cell differentiation but very weak Th1 and Th17 cell differentiation. Together, these findings reveal a TRIF-CD40-Th17 axis in the development of IL-17-associated neutrophilic asthma.
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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.