title: Increased levels of (class switched) memory B cells in peripheral blood of current smokers.
abstract: There is increasing evidence that a specific immune response contributes to the pathogenesis of COPD. B-cell follicles are present in lung tissue and increased anti-elastin titers have been found in plasma of COPD patients. Additionally, regulatory T cells (Tregs) have been implicated in its pathogenesis as they control immunological reactions. We hypothesize that the specific immune response in COPD is smoke induced, either by a direct effect of smoking or as a result of smoke-induced lung tissue destruction (i.e. formation of neo-epitopes or auto antigens). Furthermore, we propose that Tregs are involved in the suppression of this smoke-induced specific immune response.The presence of B cells, memory B cells and Tregs was assessed by flow cytometry in peripheral blood of 20 COPD patients and 29 healthy individuals and related to their current smoking status.COPD patients had lower (memory) B-cell percentages and higher Treg percentages in peripheral blood than healthy individuals, with a significant negative correlation between these cells. Interestingly, current smokers had higher percentages of (class-switched) memory B cells than ex-smokers and never smokers, irrespective of COPD.This increase in (class-switched) memory B cells in current smokers is intriguing and suggests that smoke-induced neo-antigens may be constantly induced in the lung. The negative correlation between B cells and Tregs in blood is in line with previously published observations that Tregs can suppress B cells. Future studies focusing on the presence of these (class switched) memory B cells in the lung, their antigen specificity and their interaction with Tregs are necessary to further elucidate the specific B-cell response in COPD.
authors.affiliation: Department of Pulmonary Diseases, University Medical Center Groningen, University of Groningen, 9700 RB, Groningen, The Netherlands. c.a.brandsma@path.umcg.nl
authors.forename: Corry-Anke
authors.initials: CA
authors.lastname: Brandsma
authors.forename: Machteld N
authors.initials: MN
authors.lastname: Hylkema
authors.forename: Marie
authors.initials: M
authors.lastname: Geerlings
authors.forename: Wouter H
authors.initials: WH
authors.lastname: van Geffen
authors.forename: Dirkje S
authors.initials: DS
authors.lastname: Postma
authors.forename: Wim
authors.initials: W
authors.lastname: Timens
authors.forename: Huib A M
authors.initials: HA
authors.lastname: Kerstjens
mesh_terms: D000368:Aged; D001324:Autoantigens / Q000276:immunology; D001402:B-Lymphocytes / Q000276:immunology*; D016022:Case-Control Studies; D005434:Flow Cytometry; D006801:Humans; D017578:Immunoglobulin Class Switching; D007156:Immunologic Memory; D016014:Linear Models; D008168:Lung / Q000276:immunology; D018655:Lymphocyte Count; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D012907:Smoking / Q000009:adverse effects / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
chemical_list: D001324:Autoantigens