LAUSR

Cystic fibrosis and non-cystic fibrosis bronchiectasis share as their main clinical hallmark repeated lung infections by opportunist pathogens. In the normal adult lung, almost no lymphoid tissue is observed, in contrast to fetal and paediatric lungs [1] and in contrast to upper airways [2]. Neogenesis of bronchial-associated lymphoid tissue (BALT), also referred to as induced BALT (iBALT) or ectopic lymphoid follicles, has been observed in several chronic lung diseases, including chronic obstructive pulmonary disease (COPD) [3], lung cancer [4], pulmonary hypertension [5], post-transplant restrictive allograft syndrome [6] or rheumatoid lung [7], as well as possibly, to some extent, in asthma [8]. A distinction should thus be made between aggregates of B-cells without specific reorganisation and lymphoid follicle structures as observed in primary (bone marrow, thymus) and secondary lymphoid organs (lymph nodes, spleen and Peyer's patches). Lymphoid follicles contain mature naïve and memory B-cells, T-cells, dendritic cells and follicular dendritic cells organising in germinal centres and vascularised with lymphatics and high endothelial veinules. Such lymphoid follicles in non-lymphoid organs are called mucosal-associated lymphoid tissue in mucosal tissues and tertiary lymphoid follicles in other organs. Frija-Masson and co-workers draw definite conclusions on the role of pathogens for lymphoid neogenesis in the CF lung http://ow.ly/v4iH309MbCs