van der Strate Barry W A, Postma Dirkje S, Brandsma Corry-Anke, Melgert Barbro N, Luinge Marjan A, Geerlings Marie, Hylkema Machteld N, van den Berg Anke, Timens Wim, Kerstjens Huib A M
Department of Respiratory Medicine, University Medical Center Groningen, Postbox 30.001, NL-9700-RB Groningen, The Netherlands.
Am J Respir Crit Care Med. 2006 Apr 1;173(7):751-8. doi: 10.1164/rccm.200504-594OC. Epub 2006 Jan 6.
Little is known about what drives the inflammatory reaction in the development of chronic obstructive lung disease. B cells have been found.
To study the involvement of B cells in the development of emphysema.
The presence of B-cell follicles and their interaction with other cells were investigated in lungs of patients with chronic obstructive pulmonary disease and of smoking mice. B cells were isolated from lymphoid follicles by laser microdissection and analyzed for the presence of immunoglobulin rearrangements and somatic mutations.
Lymphoid follicles consisting of B cells and follicular dendritic cells with adjacent T cells were demonstrated both in the parenchyma and in bronchial walls of patients with emphysema. A clonal process was observed in all follicles and the presence of ongoing somatic mutations was observed in 75% of the follicles, indicating oligoclonal, antigen-specific proliferation. Similar lymphoid follicles were detected in mice that had developed pulmonary inflammation and progressive alveolar airspace enlargement after smoking. The increase in the number of B-cell follicles was progressive with time and correlated with the increase in mean linear intercept. Specific bacterial or viral nucleic acids could not be detected.
B-cell follicles with an oligoclonal, antigen-specific reaction were found in men and mice with emphysema. In mice, the development was progressive with time and correlated with the increase in airspace enlargement. We hypothesize that these B cells contribute to the inflammatory process and/or the development and perpetuation of emphysema by producing antibodies against either tobacco smoke residues or extracellular matrix components.
关于慢性阻塞性肺疾病发展过程中引发炎症反应的因素所知甚少。已发现B细胞。
研究B细胞在肺气肿发展过程中的作用。
在慢性阻塞性肺疾病患者和吸烟小鼠的肺组织中，研究B细胞滤泡的存在及其与其他细胞的相互作用。通过激光显微切割从淋巴滤泡中分离出B细胞，并分析免疫球蛋白重排和体细胞突变情况。
在肺气肿患者的实质组织和支气管壁中均发现了由B细胞、滤泡树突状细胞及相邻T细胞组成的淋巴滤泡。在所有滤泡中均观察到克隆过程，75%的滤泡中存在持续的体细胞突变，表明为寡克隆、抗原特异性增殖。在吸烟后发生肺部炎症和进行性肺泡腔扩大的小鼠中也检测到了类似的淋巴滤泡。B细胞滤泡数量随时间逐渐增加，并与平均线性截距的增加相关。未检测到特定的细菌或病毒核酸。
在患有肺气肿的人和小鼠中发现了具有寡克隆、抗原特异性反应的B细胞滤泡。在小鼠中，其发展随时间而进展，并与肺泡腔扩大的增加相关。我们推测这些B细胞通过产生针对烟草烟雾残留物或细胞外基质成分的抗体，促进了炎症过程以及肺气肿的发展和持续。
