Predominance of Th1‐type T cells in synovial fluid of patients with Yersinia‐induced reactive arthritis
Predominance of Th1‐type T cells in synovial fluid of patients with Yersinia‐induced reactive arthritis
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耶尔森菌引起的关节炎反应性患者滑液中 Th1 型 T 细胞的优势
DOI：
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发表时间：
1992
影响因子：
5.4
通讯作者：
B. Fleischer
中科院分区：
文献类型：
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作者：
J. Schlaak;E. Hermann;M. Ringhoffer;P. Probst;H. Gallati;K. zum Büschenfelde;B. Fleischer
反应性关节炎的发病机制和小肠结肠炎耶尔森氏菌特异性滑膜T细胞的功能能力尚不清楚。在这项研究中，我们确定了来自2名耶尔森氏菌诱导的反应性关节炎患者的24个CD 4+滑液（SF）来源的T细胞克隆的细胞因子分泌模式，16个克隆特异于不同的耶尔森氏菌抗原，8个克隆作为对照。对耶尔森氏菌抗原特异性的克隆主要属于T辅助细胞1（Th 1）亚群，产生干扰素（IFN）-γ和白细胞介素（IL）-2，但不产生IL-4，而不与耶尔森氏菌抗原反应的SF T细胞产生IL-2、IL-4和IFN-γ，因此属于Th 0亚群。此外，从SF和外周血建立的短期T细胞系显示出相同的模式。为了进一步分析这些数据的功能相关性，我们研究了IFN-γ和IL-4对人胶质母细胞瘤细胞系中耶尔森氏菌细胞内杀伤的影响。我们的数据表明，Th 1细胞因子IFN-γ促进细胞内杀死耶尔森氏菌，而这种作用被Th 2细胞因子IL-4拮抗。此外，Th 2细胞因子IL-10抑制Th 1细胞的抗原特异性增殖反应以及IFN-γ和IL-2的产生。这些结果提供了对小肠结肠炎耶尔森菌感染后反应性关节炎中工作的抗菌机制的深入了解，并首次揭示了来自Th 1和Th 2细胞的细胞因子在人类对细菌抗原的免疫应答中的交叉调节特性。
The pathogenetic mechanisms underlying the development of reactive arthritis and the functional capacities of synovial T cells specific for Yersinia enterocolitica are still unclear. In this study we have determined the cytokine secretion patterns of 24 CD4+ synovial fluid (SF)‐derived T cell clones from 2 patients with Yersinia‐induced reactive arthritis, 16 clones specific for different Yersinia antigens and 8 clones as controls. The clones specific for Yersinia antigens predominantly belong to the T helper cell 1 (Th1) subset with production of interferon (IFN)‐γ and interleukin (IL)‐2, but no IL‐4, whereas SF T cells not reactive with Yersinia antigens produce IL‐2, IL‐4 and IFN‐γ and thus belonged to the Th0 subset. Moreover, short‐term T cell lines established from SF and peripheral blood showed the same pattern. To further analyze the functional relevance of these data we investigated the influence of IFN‐γ and IL‐4 on the intracellular killing of Yersinia in a human glioblastoma cell line. Our data show that the Th1 cytokine IFN‐γ promotes intracellular killing of Yersinia, whereas this effect is antagonized by the Th2 cytokine IL‐4. Furthermore, the Th2 cytokine IL‐10 inhibited the antigen‐specific proliferative response and IFN‐γ and IL‐2 production by the Th1 cells. These results provide insight into the antibacterial mechanisms at work in reactive arthritis after infection with Yersinia enterocolitica and, for the first time, reveal the cross‐regulatory properties of cytokines derived from Th1 and Th2 cells in a human immune response to bacterial antigens.