首页> 美国卫生研究院文献>British Journal of Experimental Pathology >Enhanced adhesion of autologous lymphocytes to gamma-interferon-treated human endothelial cells in vitro.
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Enhanced adhesion of autologous lymphocytes to gamma-interferon-treated human endothelial cells in vitro.

机译:自体淋巴细胞在体外对γ-干扰素治疗的人内皮细胞的粘附增强。

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摘要

An adhesion assay was developed using human umbilical vein endothelial cell cultures and autologous and allogeneic lymphocytes separated from cord blood. Endothelial monolayers cultured in plain or gamma-interferon (IFN gamma)-supplemented medium were cocultured with lymphocytes for 1 h and non-adherent lymphocytes removed by washing. Autologous and allogeneic lymphocytes exhibited significantly increased adhesion with IFN gamma-treated cells compared with untreated controls. The increased adhesion to IFN gamma-treated endothelial cells was significantly inhibited when autologous or allogeneic lymphocytes were pre-treated with saturating amounts of an anti-CD4 monoclonal antibody. The results indicate that IFN gamma enhances lymphocyte binding to endothelium and that the CD4 molecule may be involved in this process. This could be an important mechanism in targetting the migrating of T-helper (Th) cells to areas of chronic inflammation and in antigen presentation by endothelial cells.
机译:使用人脐静脉内皮细胞培养物和自脐带血分离的自体和同种异体淋巴细胞进行了粘附测定。将在纯素或γ-干扰素(IFNγ)补充培养基中培养的内皮单层细胞与淋巴细胞共培养1 h,并通过洗涤除去非粘附淋巴细胞。与未经处理的对照组相比,自体和同种异体淋巴细胞与IFNγ处理的细胞的粘附力显着提高。当用饱和量的抗CD4单克隆抗体预处理自体或同种异体淋巴细胞时,对IFNγ处理的内皮细胞粘附的增加会受到明显抑制。结果表明,IFNγ增强淋巴细胞与内皮的结合,而CD4分子可能参与了该过程。这可能是将T辅助细胞(Th)迁移到慢性炎症区域以及内皮细胞呈递抗原的重要机制。

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