ArticleFrontiers in immunology2020
Inducible Bronchus-Associated Lymphoid Tissue (iBALT) Attenuates Pulmonary Pathology in a Mouse Model of Allergic Airway Disease.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Immunological mechanistic action of intravenous BCG-mediated protection against tuberculosis.Cellular and molecular life sciences : CMLS · 2026Review
- Integrin β3 deficiency unleashes spontaneous pulmonary inflammation by promoting B cell hyperactivation via the CD40-CD40L axis.Frontiers in immunology · 2026Article
- CXCL13 and IL-33 as Immunomodulatory Adjuvants Combined with Respiratory Syncytial Virus Fusion (RSV F) Protein to Enhance Mucosal RSV Vaccination.Infection and drug resistance · 2026Review
- Lung Lymphatics in Edema, Inflammation, and Thrombosis.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- Bronchus-associated lymphoid tissue: a review of its development and function, including recent findings on the impact of environmental particulate exposure.Clinical and experimental medicine · 2025Review
- Tertiary lymphoid structures support the development of allergen-specific progenitor CD4+ T cells.bioRxiv : the preprint server for biology · 2025Article
- The roles of tertiary lymphoid structures in orchestrating immune responses in peripheral organs.Inflammation and regeneration · 2025Review
- Tertiary Lymphoid Structures in Tuberculosis: Persistence, Protection, and Pathology.Immunological reviews · 2025Review
- Characterization of bronchus-associated lymphoid tissue induced by co-exposure to Asian sand dust and ovalbumin: a study using 3D serial section imaging.Frontiers in immunology · 2025Article
- Immunomodulatory biomaterials for treating chronic inflammation at mucosal sites.npj biomedical innovations · 2025Review
- The impact of mycobacteria-induced trained immunity on SARS-CoV-2 vaccine responses.Frontiers in immunology · 2025Article
- Immune cell regulatory networks in chronic obstructive pulmonary disease: mechanistic analysis from innate to adaptive immunity.Frontiers in immunology · 2025Review
- Macrophages Orchestrate Airway Inflammation, Remodeling, and Resolution in Asthma.International journal of molecular sciences · 2023Review
- The lymphatic vasculature in lung function and respiratory disease.Frontiers in medicine · 2023Review
- CD4Frontiers in immunology · 2023Article
- DEPs Induce Local Ige Class Switching Independent of Their Ability to Stimulate iBALT de Novo Formation.International journal of environmental research and public health · 2022Article
- Murine Respiratory Tract Infection with Classical Klebsiella pneumoniae Induces Bronchus-Associated Lymphoid Tissue.Infection and immunity · 2022Article
- Leveraging Antibody, B Cell and Fc Receptor Interactions to Understand Heterogeneous Immune Responses in Tuberculosis.Frontiers in immunology · 2022Review
- Apoptosis of Eosinophil Granulocytes.Biology · 2020Review
- Short histological kaleidoscope - recent findings in histology. Part II.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Inducible Bronchus Associated Lymphoid Tissue (iBALT) is an ectopic lymphoid tissue associated with severe forms of chronic lung diseases, including chronic obstructive pulmonary disease, rheumatoid lung disease, hypersensitivity pneumonitis and asthma, suggesting that iBALT may exacerbate these clinical conditions. However, despite the link between pulmonary pathology and iBALT formation, the role of iBALT in pathogenesis remains unknown. Here we tested whether the presence of iBALT in the lung prior to sensitization and challenge with a pulmonary allergen altered the biological outcome of disease. We found that the presence of iBALT did not exacerbate Th2 responses to pulmonary sensitization with ovalbumin. Instead, we found that mice with iBALT exhibited delayed Th2 accumulation in the lung, reduced eosinophil recruitment, reduced goblet cell hyperplasia and reduced mucus production. The presence of iBALT did not alter Th2 priming, but instead delayed the accumulation of Th2 cells in the lung following challenge and altered the spatial distribution of T cells in the lung. These results suggest that the formation of iBALT and sequestration of effector T cells in the context of chronic pulmonary inflammation may be a mechanism by which the immune system attenuates pulmonary inflammation and prevents excessive pathology.
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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.