Desmetz Caroline, Lin Yea-Lih, Mettling Clément, Portalès Pierre, Noël Danièle, Clot Jacques, Jorgensen Christian, Corbeau Pierre
Institut de Génétique Humaine du CNRS UPR1142, Montpellier, F-34000, France.
Clin Immunol. 2007 May;123(2):148-54. doi: 10.1016/j.clim.2007.01.004. Epub 2007 Mar 23.
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.
由于我们最近发现细胞表面CCR5分子的数量决定了其作为趋化因子受体的功能效率,我们检验了以下假设:细胞表面CCR5密度可能会影响T淋巴细胞募集到类风湿性关节中的强度。为此,我们建立了两个源自Jurkat细胞系的克隆,它们仅在细胞表面CCR5密度上有所不同。我们研究了它们对TNF-α转导的类风湿性滑膜细胞上清液的趋化性。与表达较低表面CCR5密度的Jurkat细胞亚系相比,表达较高细胞表面CCR5密度的Jurkat细胞亚系对TNF-α转导的滑膜细胞上清液的迁移更强烈。此外,这种迁移被抗CCR5单克隆抗体阻断。因此,T细胞表面的CCR5密度对于给定个体而言随时间保持恒定,但在个体之间差异很大,这可能是决定类风湿关节炎病程中关节炎症强度的一个因素。