Role of iBALT in Respiratory Immunity
Pulmonary respiration inevitably exposes the mucosal surface of the lung to potentially noxious stimuli, including pathogens, allergens, and particulates, each of which can trigger pulmonary damage and inflammation. As inflammation resolves, B and T lymph
- PDF / 508,749 Bytes
- 23 Pages / 439.37 x 666.142 pts Page_size
- 41 Downloads / 197 Views
Contents 1 Introduction.......................................................................................................................... 2 Mechanisms Leading to iBALT Formation: A Rainbow of Options ................................ 3 Role of iBALT in Immunity Against Infectious Diseases ................................................. 4 Role of iBALT in the Immune Response Against Non-infectious Agents ....................... 5 Conclusion ........................................................................................................................... References ..................................................................................................................................
Abstract Pulmonary respiration inevitably exposes the mucosal surface of the lung to potentially noxious stimuli, including pathogens, allergens, and particulates, each of which can trigger pulmonary damage and inflammation. As inflammation resolves, B and T lymphocytes often aggregate around large bronchi to form inducible Bronchus-Associated Lymphoid Tissue (iBALT). iBALT formation can be initiated by a diverse array of molecular pathways that converge on the activation and differentiation of chemokine-expressing stromal cells that serve as the scaffolding for iBALT and facilitate the recruitment, retention, and organization of leukocytes. Like conventional lymphoid organs, iBALT recruits naïve lymphocytes from the blood, exposes them to local antigens, in this case from the airways, and supports their activation and differentiation into effector cells. The activity of iBALT is demonstrably beneficial for the clearance of respiratory pathogens; however, it is less clear whether it dampens or exacerbates inflammatory responses to non-infectious agents. Here, we review the evidence regarding the role of iBALT in pulmonary immunity and propose that the final outcome depends on the context of the disease. A. Silva-Sanchez T. D. Randall (&) Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, 1720 2nd AVE S, Birmingham, AL 35294, USA e-mail: [email protected] Current Topics in Microbiology and Immunology https://doi.org/10.1007/82_2019_191 © Springer Nature Switzerland AG 2019
2
A. Silva-Sanchez and T. D. Randall
1 Introduction Lymph nodes (LNs) are small, bean-shaped organs found along lymphatic vessels that drain the parenchyma of non-lymphoid organs. Like other secondary lymphoid organs (SLOs), LNs have a characteristic lymphoid architecture, with segregated B and T cell domains organized by distinct stromal cell types (Fletcher et al. 2011; Gentek and Bajenoff 2017). This structure facilitates the encounter of rare, antigen-specific lymphocytes with antigen-bearing dendritic cells (DCs) and thereby supports primary immune responses (Flajnik 2002; Neely and Flajnik 2016). LN formation occurs during late embryogenesis according to a developmental program that proceeds independently of antigen or inflammation (Luther et al. 2003). However, lymphocytes
Data Loading...
