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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Cell surface CCR5 density determines the intensity of T cell migration towards rheumatoid arthritis synoviocytes.
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Cell surface CCR5 density determines the intensity of T cell migration towards rheumatoid arthritis synoviocytes.

机译：细胞表面CCR5密度决定了T细胞向类风湿关节炎滑膜细胞迁移的强度。

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摘要

As we have recently shown that the number of CCR5 molecules at the cell surface determines the efficiency of its function as a chemokine receptor, we tested the hypothesis that cell surface CCR5 density could influence the intensity of T lymphocyte recruitment into the rheumatoid joint. For this purpose, we established two Jurkat cell line-derived clones that differed only by their cell surface CCR5 densities. We studied their chemotaxis towards TNF-alpha-transduced rheumatoid synoviocytes supernatant. The Jurkat cell subline that expressed the higher cell surface CCR5 density migrated more intensively towards the supernatant of TNF-alpha-transduced synoviocytes than the Jurkat cell subline that expressed a lower surface CCR5 density. Moreover, this migration was blocked by an anti-CCR5 mAb. The CCR5 density on T cell surface, which is constant over time for a given individual, but varies drastically from one individual to another, might thus be a factor determining the intensity of joint inflammation in the course of RA.
机译：正如我们最近显示的，细胞表面CCR5分子的数量决定了其作为趋化因子受体的功能的效率，我们测试了细胞表面CCR5密度可能影响T淋巴细胞向类风湿关节募集强度的假设。为此，我们建立了两个Jurkat细胞系衍生的克隆，它们的区别仅在于其细胞表面CCR5密度。我们研究了它们对TNF-α转导的类风湿滑膜细胞上清液的趋化性。表达较高细胞表面CCR5密度的Jurkat细胞亚系比表达较低表面CCR5密度的Jurkat细胞亚系更密集地向TNF-α转导的滑膜细胞上清迁移。此外，这种迁移被抗CCR5 mAb阻断。对于一个给定的个体，T细胞表面的CCR5密度随时间变化是恒定的，但一个个体之间的变化却很大，因此可能是决定RA过程中关节炎症强度的因素。

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