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.
Highlights
COPD is a leading cause of death worldwide and its morbidity and mortality are still rising
Increased numbers of CD4+CD25bright Tregs were shown in bronchoalveolar lavage (BAL) from COPD patients and healthy smokers compared to healthy never smokers [13], while another group showed decreased CD4+CD25+ Tregs in BAL of COPD patients and never smokers compared to healthy smokers [14]
An immunohistochemical study demonstrated increased numbers of Foxp3+ cells in large airways of asymptomatic smokers and COPD patients compared to non-smokers, and decreased numbers of Foxp3+ cells in small airways of COPD patients compared to asymptomatic smokers and non-smokers [15]
Summary
COPD is a leading cause of death worldwide and its morbidity and mortality are still rising. The only effective treatment to stop the accelerated lung function decline is smoking cessation, even though the inflammatory response may persist [1]. More information is needed about the origins and nature of the chronic inflammatory response in COPD to find better treatment targets for COPD patients. Increased numbers of CD4+CD25bright Tregs were shown in BAL from COPD patients and healthy smokers compared to healthy never smokers [13], while another group showed decreased CD4+CD25+ Tregs in BAL of COPD patients and never smokers compared to healthy smokers [14]. An immunohistochemical study demonstrated increased numbers of Foxp3+ cells in large airways of asymptomatic smokers and COPD patients compared to non-smokers, and decreased numbers of Foxp3+ cells in small airways of COPD patients compared to asymptomatic smokers and non-smokers [15]
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