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ST2在恶性胸腔积液辅助性T淋巴细胞中的表达

Expression of ST2 in helper T lymphocytes of malignant pleural effusions.

作者信息

Oshikawa Katsuhisa, Yanagisawa Ken, Ohno Shoji, Tominaga Shin-Ichi, Sugiyama Yukihiko

机构信息

Division of Pulmonary Medicine, Department of Medicine, Jichi Medical School, Minamikawachi, Tochigi, Japan.

出版信息

Am J Respir Crit Care Med. 2002 Apr 1;165(7):1005-9. doi: 10.1164/ajrccm.165.7.2105109.

DOI:10.1164/ajrccm.165.7.2105109
PMID:11934729
Abstract

The objective of this study was to test the hypothesis that accumulated helper T lymphocytes in malignant pleural effusions may shift to T-helper type 2 (Th2) and produce soluble ST2 protein. We took samples of serum and pleural effusions (p-) from patients with carcinomatous pleurisy (CA, n = 17), tuberculous pleurisy (TB, n = 8), and congestive heart failure (HF, n = 5) and compared the concentration of cytokines or ST2. Ex vivo production of interleukin (IL)-4 and IL-10, though not that of interferon (IFN)-gamma or IL-12, from CD4+ T cells isolated from pleural effusions was higher in the CA group than in the TB or HF group. The p-ST2 concentrations were significantly higher in the CA group than in the TB or HF group, positively correlated with the percentage of pleural effusion CD4+ T cells (r = 0.432, p = 0.016) and inversely correlated with p-IFN-gamma concentrations (r = -0.423, p = 0.019). Furthermore, mRNA expression of ST2 in CD4+ T cells isolated from group CA was upregulated, compared with that in those isolated from the TB group. These results suggest that CD4+ T cells in CA shift to Th2, which can produce soluble ST2 protein, resulting in increased concentrations of p-ST2 in malignant pleural effusion.

摘要

本研究的目的是检验以下假设

恶性胸腔积液中积累的辅助性T淋巴细胞可能转变为2型辅助性T细胞(Th2)并产生可溶性ST2蛋白。我们采集了癌性胸膜炎(CA,n = 17)、结核性胸膜炎(TB,n = 8)和充血性心力衰竭(HF,n = 5)患者的血清和胸腔积液样本(p-),并比较了细胞因子或ST2的浓度。与TB组或HF组相比,CA组从胸腔积液中分离出的CD4 + T细胞产生白细胞介素(IL)-4和IL-10的体外产量较高,而干扰素(IFN)-γ或IL-12的产量则不然。CA组的p-ST2浓度显著高于TB组或HF组,与胸腔积液CD4 + T细胞百分比呈正相关(r = 0.432,p = 0.016),与p-IFN-γ浓度呈负相关(r = -0.423,p = 0.019)。此外,与从TB组分离出的CD4 + T细胞相比,从CA组分离出的CD4 + T细胞中ST2的mRNA表达上调。这些结果表明,CA中的CD4 + T细胞转变为Th2,后者可产生可溶性ST2蛋白,导致恶性胸腔积液中p-ST2浓度升高。

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