Expression of TIM-3 on CD4+ and CD8+ T cells in the peripheral blood and synovial fluid of rheumatoid arthritis

Expression of TIM-3 on CD4+ and CD8+ T cells in the peripheral blood and synovial fluid of rheumatoid arthritis
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DOI：
10.1111/apm.12228
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发表时间：
2014-10-01
期刊：
APMIS
影响因子：
2.8
通讯作者：
Zhang, Ming
Zhang, Ming
中科院分区：
医学3区
文献类型：
--
作者：
Li, Shufeng;Peng, Dayong;Zhang, Ming

文献摘要

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相似文献

类风湿性关节炎 (RA) 的特征是针对关节关节滑膜内层的慢性炎症过程。 TIM-3在免疫反应的负调节中发挥着关键作用。在本研究中，我们从 RA 的全身（外周血）和局部（滑液）角度研究了 TIM-3 在 CD4+ 和 CD8+ T 细胞上的表达。通过流式细胞术测量患者外周血和滑液以及健康对照外周血中TIM-3+细胞的水平。结果显示，RA 外周血 CD4+ 和 CD8+ T 细胞中 TIM-3 表达显着增加（分别为 p < 0.001 和 p < 0.001）。此外，患者滑液中 CD4+ 和 CD8+ T 细胞的 TIM-3 表达甚至高于外周血中的表达。当将 TIM-3 水平与 RA 严重程度进行比较时，我们发现外周 CD4+ 和外周 CD8+ T 细胞上的 TIM-3 百分比与患者的疾病活动评分 28 (DAS28) 呈负相关。同样，滑液 CD4+ 和 CD8+ T 细胞上的 TIM-3 也显示与病例的 DAS28 呈负相关。我们的数据表明 TIM-3 与 RA 疾病进展之间呈负相关。
Rheumatoid arthritis (RA) is characterized by a chronic inflammatory process that targets the synovial lining of diarthrodial joints. TIM-3 plays a key role in the negative regulation of the immune response. In this study, we investigated the expression of TIM-3 on CD4+ and CD8+ T cells from systemic (peripheral blood) and local (synovial fluid) perspectives of RA. Level of TIM-3+ cells from peripheral blood and synovial fluid of patients as well as peripheral blood of healthy controls was measured by flow cytometry. Results showed that TIM-3 expression was significantly increased in both CD4+ and CD8+ T cells in the peripheral blood of RA (p < 0.001 and p < 0.001, respectively). Furthermore, patients revealed even higher expression of TIM-3 in CD4+ and CD8+ T cells in synovial fluid than in peripheral blood. When comparing TIM-3 level with the severity of RA, we identified that the percentage of TIM-3 on both peripheral CD4+ and peripheral CD8+ T cells was negatively correlated with disease activity score 28 (DAS28) of the patients. Similarly, TIM-3 on synovial fluid CD4+ and CD8+ T cells also revealed inverse correlation with DAS28 of the cases. Our data demonstrate a negative correlation between TIM-3 and the disease progression of RA.