Invariant natural killer T cells in chronic obstructive pulmonary disease
Invariant natural killer T cells in chronic obstructive pulmonary disease
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DOI：
10.1111/j.1440-1843.2011.02104.x
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发表时间：
2012-04-01
期刊：
影响因子：
6.9
通讯作者：
Lim, Sung Chul
中科院分区：
文献类型：
--
作者：
Chi, Su Young;Ban, Hee Jung;Lim, Sung Chul
背景和目的：慢性阻塞性肺疾病（COPD）患者的先天性和获得性免疫系统中，不变性自然杀伤T（iNKT）细胞可能起着重要的调节作用。然而，关于iNKT细胞在COPD发病机制中的潜在作用的信息很少。为了探讨iNKT细胞是否在COPD中发挥重要作用，对28例COPD患者和19例年龄匹配的健康对照者外周血中iNKT细胞的频率进行了分析。用6 B11 mAb、抗T细胞受体V α 24 mAb、抗T细胞受体V β 11 mAb或负载α-半乳糖神经酰胺的CD 1d四聚体对血液iNKT细胞进行染色，并通过流式细胞术进行分析。结果：CD4（+）6B11（+）iNKT、CD4+ V α 24（+）iNKT COPD患者外周血中CD 4（+）V β 11（+）iNKT和CD 3（+）6 B11（+）iNKT细胞显著低于健康对照组。COPD急性加重期患者外周血中CD 4（+）6 B11（+）iNKT细胞频率较COPD稳定期患者明显降低。这些结果有力地表明，iNKT细胞可能在COPD的发病机制中发挥重要作用。
Background and objective: Invariant natural killer T (iNKT) cells may play an important role in regulating the innate and acquired immune systems in chronic obstructive pulmonary disease (COPD). However, there is little information regarding the potential role of iNKT cells in the pathogenesis of COPD. To investigate whether iNKT cells have an important role in COPD, the frequency of iNKT cells in peripheral blood of patients with COPD was analysed.Methods: This was a comparative study of 28 patients with COPD and 19 age-matched healthy control subjects. Blood iNKT cells were stained with 6B11 mAb, anti-T cell receptor V alpha 24 mAb, anti-T cell receptor V beta 11 mAb or a-galactosylceramide-loaded CD1d-tetramer, and analysed by flow cytometry.Results: The frequency of CD4(+) 6B11(+) iNKT, CD4+ V alpha 24(+) iNKT, CD4(+) V beta 11(+) iNKT and CD3(+) 6B11(+) iNKT cells was significantly lower in peripheral blood of patients with COPD than in that of healthy control subjects. The frequency of CD4(+) 6B11(+) iNKT cells was significantly lower in patients with exacerbations of COPD compared with those with stable COPD.Conclusions: The frequency of iNKT was decreased in peripheral blood of patients with COPD. These results strongly suggest that iNKT cells may play an important role in the pathogenesis of COPD.