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.
Highlights
Inducible Bronchus Associated Lymphoid Tissue is an ectopic lymphoid tissue that forms in the lung following inflammation or infection [1, 2]
Given that germinal centers (GCs) only form in organized lymphoid tissues, we conclude that pulmonary exposure of neonates to LPS promotes the formation of functional Inducible Bronchus Associated Lymphoid Tissue (iBALT) areas
The spatial distribution of effector T cells is altered by the presence of iBALT, such that effector CD4 T cells as well as Tregs become concentrated in iBALT areas and relatively diluted in the rest of the lung
Summary
Inducible Bronchus Associated Lymphoid Tissue (iBALT) is an ectopic lymphoid tissue that forms in the lung following inflammation or infection [1, 2]. IBALT is not encapsulated, but is instead embedded in the lung tissue, most often along large bronchi or filling the peri-vascular space of pulmonary artieries [4, 5]. Despite being in a mucosal tissue, iBALT often lacks a welldefined M cell-containing dome epithelium [6] and its high endothelial venules (HEVs) express peripheral lymph node addressin (PNAd) [7] rather than mucosal addressin cell adhesion molecule iBALT Regulates Pulmonary Th2 Responses (MAdCAM). IBALT clearly participates in pulmonary mucosal immune responses, it lacks some of the features often associated with classic mucosal lymphoid organs. Unlike conventional lymphoid organs, which develop independently of antigen during embryogenesis [8, 9], iBALT forms following pulmonary infection or inflammation [10, 11]. The neonatal period is the same developmental window when microbial exposure, or lack thereof, imprints the immune system to be more or less susceptible to developing atopic responses to foreign antigens [17, 18] or developing autoreactive responses to self antgens—the so—called hygiene effect
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