Department of Pulmonary Diseases, University Medical Center Groningen, University of Groningen, 9700 RB, Groningen, The Netherlands.
Respir Res. 2009 Nov 12;10(1):108. doi: 10.1186/1465-9921-10-108.
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.
越来越多的证据表明，特定的免疫反应有助于 COPD 的发病机制。B 细胞滤泡存在于肺组织中，并且在 COPD 患者的血浆中发现了抗弹性蛋白滴度增加。此外，调节性 T 细胞（Tregs）也与发病机制有关，因为它们控制着免疫反应。我们假设 COPD 中的特定免疫反应是由吸烟引起的，可能是吸烟的直接作用，也可能是由于吸烟引起的肺组织破坏（即形成新表位或自身抗原）。此外，我们提出 Tregs 参与了这种由烟雾引起的特定免疫反应的抑制。通过流式细胞术评估了 20 名 COPD 患者和 29 名健康个体外周血中的 B 细胞、记忆 B 细胞和 Tregs 的存在，并将其与他们当前的吸烟状况相关联。COPD 患者外周血中的（记忆）B 细胞百分比和 Treg 百分比低于健康个体，并且这些细胞之间存在显著的负相关。有趣的是，当前吸烟者的（类别转换）记忆 B 细胞百分比高于前吸烟者和从不吸烟者，无论是否患有 COPD。当前吸烟者中（类别转换）记忆 B 细胞的这种增加令人感兴趣，表明烟雾诱导的新抗原可能在肺部不断产生。血液中 B 细胞和 Tregs 之间的负相关与之前发表的观察结果一致，即 Tregs 可以抑制 B 细胞。需要进一步阐明 COPD 中特定的 B 细胞反应，因此需要进一步研究这些（类别转换）记忆 B 细胞在肺部的存在、它们的抗原特异性及其与 Tregs 的相互作用。
