Horner A, Davies M E, Franz B
Strangeways Research Laboratory, Worts Causeway, Cambridge, UK.
Immunology. 1995 Dec;86(4):584-90.
Chondrocytes express a number of cell-surface molecules that mediate cell-cell or cell-matrix interactions. The expression of intercellular adhesion molecule-1 (ICAM-1) by chondrocytes under inflammatory conditions has been well documented. Here we demonstrate the involvement of ICAM-1-, CD18- and RGD-dependent adhesion mechanisms in chondrocyte-T-cell adhesion and in cell-mediated killing of chondrocytes in vitro. In the absence of cytokine stimulation, chondrocyte-peripheral blood mononuclear cell (PBMC) interactions were unaffected by inhibition of ICAM-1-dependent pathways but were significantly reduced by blockade of CD18- and RGD-dependent pathways. Following cytokine stimulation chondrocyte-PBMC adhesion and chondrocyte killing were significantly increased. These effects could be inhibited by the blockade of ICAM-1.
软骨细胞表达多种介导细胞间或细胞与基质相互作用的细胞表面分子。在炎症条件下软骨细胞表达细胞间黏附分子-1(ICAM-1)已得到充分证明。在此我们证明ICAM-1、CD18和RGD依赖性黏附机制参与体外软骨细胞与T细胞的黏附以及细胞介导的软骨细胞杀伤。在没有细胞因子刺激的情况下,软骨细胞与外周血单核细胞(PBMC)的相互作用不受ICAM-1依赖性途径抑制的影响,但CD18和RGD依赖性途径的阻断会使其显著降低。细胞因子刺激后,软骨细胞与PBMC的黏附及软骨细胞杀伤显著增加。这些效应可被ICAM-1的阻断所抑制。