Cigarette smoke-induced iBALT mediates macrophage activation in a B cell-dependent manner in COPD

ABSTRACT: 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 pathogenesis 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, as well as 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 increased lung compliance, total lung capacity, and mean linear chord length in WT, but not B cell-deficient mice, associated with an increased size and

ORGANISM(S): Mus musculus

SUBMITTER: Johannes Beckers 

PROVIDER: E-GEOD-52509 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress