Institute of Respiratory Diseases, First Affiliated Hospital, Guangxi Medical University, Nanning, China.
Respirology. 2010 Apr;15(3):522-9. doi: 10.1111/j.1440-1843.2010.01719.x. Epub 2010 Mar 19.
CD4(+)CD25(high) regulatory T cells are increased in tuberculous pleural effusions (TPE). However, the mechanism by which CD4(+)CD25(high) T cells infiltrate into the pleural cavity is unknown. The aim of this study was to investigate whether the chemokines CCL22 and CCL17 are present in TPE, and the chemoattractant activity of these chemokines for infiltration of CD4(+)CD25(high) T cells into the pleural space.
The concentrations of CCL22 and CCL17 were measured in pleural effusions from 33 patients with tuberculous pleurisy, 21 patients with pleural bacterial infections and 18 patients with transudative pleural effusions. T lymphocyte subsets in pleural effusions were assessed by flow cytometry. Pleural effusion cells were analysed for the expression of CCL22. The chemoattractant activity of CCL22 for CD4(+)CD25(high) T cells was assessed in vitro.
The frequency of CD4(+)CD25(high) T cells was significantly higher in TPE than in blood. High concentrations of CCL22 were detected in tuberculous effusions, but not in bacterial effusions or transudates. Macrophages and T cells in TPE expressed CCL22. Tuberculous pleural fluid was chemotactic for CD4(+)CD25(high) T cells in vitro, and anti-CCL22 antibody partly inhibited this chemotactic activity.
CCL22 appeared to be increased in TPE compared with bacterial pleural effusions or transudates. CCL22 may be responsible for the infiltration of CD4(+)CD25(high) T cells into the pleural space of patients with tuberculous pleurisy.
CD4(+)CD25(high)调节性 T 细胞在结核性胸腔积液（TPE）中增加。然而，CD4(+)CD25(high)T 细胞浸润胸腔的机制尚不清楚。本研究旨在探讨趋化因子 CCL22 和 CCL17 是否存在于 TPE 中，以及这些趋化因子对 CD4(+)CD25(high)T 细胞浸润胸腔的趋化活性。
测量 33 例结核性胸膜炎、21 例胸膜细菌感染和 18 例渗出性胸腔积液患者胸腔积液中的 CCL22 和 CCL17 浓度。通过流式细胞术评估胸腔积液中的 T 淋巴细胞亚群。分析胸腔积液细胞中 CCL22 的表达。体外评估 CCL22 对 CD4(+)CD25(high)T 细胞的趋化活性。
TPE 中 CD4(+)CD25(high)T 细胞的频率明显高于血液。结核性渗出液中检测到高浓度的 CCL22，但在细菌性渗出液或漏出液中未检测到。TPE 中的巨噬细胞和 T 细胞表达 CCL22。结核性胸腔积液在体外对 CD4(+)CD25(high)T 细胞具有趋化活性，抗 CCL22 抗体部分抑制了这种趋化活性。
与细菌性胸腔积液或漏出液相比，CCL22 似乎在 TPE 中增加。CCL22 可能是导致结核性胸膜炎患者 CD4(+)CD25(high)T 细胞浸润胸腔的原因。
