Enhanced adhesion of autologous lymphocytes to gamma-interferon-treated human endothelial cells in vitro.

M H Thornhill, D M Williams, P M Speight
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Abstract

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.

体外增强自体淋巴细胞对γ -干扰素处理的人内皮细胞的粘附。
利用人脐静脉内皮细胞培养物和从脐带血中分离的自体和异体淋巴细胞,建立了一种粘附试验。在普通或γ -干扰素(IFN γ)补充培养基中培养的内皮单层与淋巴细胞共培养1小时,洗涤去除非粘附淋巴细胞。与未处理的对照组相比,自体和异体淋巴细胞与IFN γ处理细胞的粘附性显著增加。当自体或异体淋巴细胞用饱和量的抗cd4单克隆抗体预处理时,对IFN γ处理的内皮细胞的粘附性增加被显著抑制。结果表明IFN γ增强了淋巴细胞与内皮细胞的结合,CD4分子可能参与了这一过程。这可能是靶向t辅助细胞迁移到慢性炎症区域和内皮细胞抗原呈递的重要机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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