Differential switching to IgG and IgA in active smoking COPD patients and healthy controls

Differential switching to IgG and IgA in active smoking COPD patients and healthy controls
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DOI:
10.1183/09031936.00011211
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发表时间:
2012-08-01
影响因子:
24.3
通讯作者:
Timens, Wim
Timens, Wim
中科院分区:
医学1区
文献类型:
--
作者:
Brandsma, Corry-Anke;Kerstjens, Huib A. M.;Timens, Wim

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多项研究表明,慢性阻塞性肺疾病 (COPD) 中存在 B 细胞滤泡和自身抗体。目前尚不清楚这种 B 细胞反应针对哪些抗原,以及它是否会导致疾病的发展或恶化。我们评估了 COPD 患者和对照者的血液和肺组织中的不同 B 细胞亚群,并比较了 B 细胞对肺部特异性抗原刺激的反应差异。主动吸烟诱导了适应性免疫反应,血液中的(类别转换)记忆 B 细胞和肺中的免疫球蛋白 (Ig)G 记忆 B 细胞水平相对较高。慢性阻塞性肺病吸烟者更多地转向 IgG,而健康吸烟者更多地转向 IgA。与健康对照相比,慢性阻塞性肺病患者肺部的记忆 B 细胞水平较高,并且与健康对照相比,用肺部特异性抗原刺激可诱导产生更多数量的抗核心蛋白聚糖抗体的细胞。 IgG 和 IgA 的差异转换表明,慢性阻塞性肺病患者和健康对照之间对烟雾的适应性免疫反应不同。 COPD 患者肺部较高水平的记忆 B 细胞可能反映了抗原特异性免疫反应,该免疫反应可能针对核心蛋白聚糖,正如 COPD 患者响应抗原特异性刺激而诱导产生抗核心蛋白聚糖抗体的细胞所表明的那样。
Several studies have demonstrated the presence of B-cell follicles and autoantibodies in chronic obstructive pulmonary disease (COPD). It is unclear against which antigens this B-cell response is directed and whether it contributes to development or worsening of disease.We assessed different B-cell subsets in blood and lung tissue from COPD patients and controls, and compared differences in B-cell responsiveness to stimulation with lung-specific antigens.Active smoking induced an adaptive immune response with relatively high levels of (class-switched) memory B-cells in blood and immunoglobulin (Ig)G memory B-cells in the lung. COPD smokers showed more switching to IgG, whereas healthy smokers switched more to IgA. COPD patients had higher levels of memory B-cells in the lung and stimulation with lung-specific antigens induced higher numbers of anti-decorin antibody-producing cells in COPD patients compared with healthy controls.Differential switching to IgG and IgA indicates that the adaptive immune response to smoke differs between COPD patients and healthy controls. A higher level of memory B-cells in the lungs of COPD patients may reflect an antigen-specific immune response, which could be directed against decorin, as suggested by the induction of anti-decorin antibody-producing cells in response to antigen-specific stimulation in COPD patients.