{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,19]],"date-time":"2026-09-19T20:22:40Z","timestamp":1789849360085,"version":"4.0.1"},"reference-count":59,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2014,11,1]]},"abstract":"<jats:p>Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures and macrophages accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. Here, we demonstrate that B cell-deficient mice are significantly protected against CS-induced emphysema. Chronic CS exposure led to an increased size and number of iBALT structures, and increased lung compliance and mean linear chord length in wild-type (WT) but not in B cell-deficient mice. The increased accumulation of lung resident macrophages around iBALT and in emphysematous alveolar areas in CS-exposed WT mice coincided with upregulated MMP12 expression. In vitro coculture experiments using B cells and macrophages demonstrated that B cell-derived IL-10 drives macrophage activation and MMP12 upregulation, which could be inhibited by an anti-IL-10 antibody. In summary, B cell function in iBALT formation seems necessary for macrophage activation and tissue destruction in CS-induced emphysema and possibly provides a new target for therapeutic intervention in COPD.<\/jats:p>","DOI":"10.1152\/ajplung.00092.2014","type":"journal-article","created":{"date-parts":[[2014,8,16]],"date-time":"2014-08-16T01:13:33Z","timestamp":1408151613000},"page":"L692-L706","source":"Crossref","is-referenced-by-count":90,"title":["Cigarette smoke-induced iBALT mediates macrophage activation in a B cell-dependent manner in COPD"],"prefix":"10.1152","volume":"307","author":[{"given":"Gerrit","family":"John-Schuster","sequence":"first","affiliation":[{"name":"Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Helmholtz Zentrum M\u00fcnchen, Member of the German Center for Lung Research, Neuherberg, 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