About this Research Topic
Lung diseases are extremely common worldwide and the recent COVID pandemic has highlighted the importance of understanding the initiation and development of pulmonary immunity. The pulmonary immune system plays a critical role not only in preventing disease but also in the development of disease. This article collection will bring together the most recent research focusing on the pathogenesis, prevention and treatment of lung disease.
Research into this area has encountered some challenges. The anatomical location of inducible bronchus-associated lymphoid tissue (iBALT) and the development of iBALT during the natural life span remain poorly documented. Most of our current knowledge of the system is acquired from the study of animal models, especially rodents, so its translational relevance needs to be investigated. There is an urgent need to study pulmonary immunity using non-human primates as a more closely related disease model to address this critical knowledge gap. In years to come, this expanded knowledge will hopefully change the way clinicians approach the treatment of lung disease during their daily practice of medicine.
In this research topic, our primary aim is to deepen our understanding of pulmonary immunity, focusing on the role of inducible bronchus-associated lymphoid tissue (iBALT) in lung diseases as studied using non-human primates. We welcome the submission of original research, reviews, mini-reviews, benchmarking analyses, and perspective articles that cover the following issues:
• Mechanisms of iBALT Regulation
• Innate Immune Sensing in the Lung
• Impact of iBALT Dynamics on Pulmonary Immunity
• Impact of age on iBALT regulation and development
• Interaction between Innate and Adaptive Immunity in Lung Diseases
• Dynamic of Pulmonary immunity during Lung Diseases
• The potential of mucosal vaccines to induce iBALT and improve the lung immune responses to other pathogens
• Using iBALT to potentiate anti-tumor immune responses.
• The role of iBALT in Th2-driven lung inflammation or asthma and allergies
Research into this area has encountered some challenges. The anatomical location of inducible bronchus-associated lymphoid tissue (iBALT) and the development of iBALT during the natural life span remain poorly documented. Most of our current knowledge of the system is acquired from the study of animal models, especially rodents, so its translational relevance needs to be investigated. There is an urgent need to study pulmonary immunity using non-human primates as a more closely related disease model to address this critical knowledge gap. In years to come, this expanded knowledge will hopefully change the way clinicians approach the treatment of lung disease during their daily practice of medicine.
In this research topic, our primary aim is to deepen our understanding of pulmonary immunity, focusing on the role of inducible bronchus-associated lymphoid tissue (iBALT) in lung diseases as studied using non-human primates. We welcome the submission of original research, reviews, mini-reviews, benchmarking analyses, and perspective articles that cover the following issues:
• Mechanisms of iBALT Regulation
• Innate Immune Sensing in the Lung
• Impact of iBALT Dynamics on Pulmonary Immunity
• Impact of age on iBALT regulation and development
• Interaction between Innate and Adaptive Immunity in Lung Diseases
• Dynamic of Pulmonary immunity during Lung Diseases
• The potential of mucosal vaccines to induce iBALT and improve the lung immune responses to other pathogens
• Using iBALT to potentiate anti-tumor immune responses.
• The role of iBALT in Th2-driven lung inflammation or asthma and allergies
Keywords: iBALT, lung disease, pulmonary immunity, non-human primate, mucosal immunity
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
