Lindsley H B, Smith D D, Cohick C B, Koch A E, Davis L S
Department of Medicine, University of Kansas Medical Center, Kansas City 66160.
Clin Immunol Immunopathol. 1993 Sep;68(3):311-20. doi: 10.1006/clin.1993.1132.
We determined the ability of proinflammatory cytokines to enhance ICAM-1 (CD54) expression on, and PBMC adhesion to, human synoviocytes. Surface molecules were characterized by cell ELISA and by flow cytometry. Adhesion of PBMC to synoviocyte monolayers was measured by direct counting or by colorimetric staining. Most cytokines upregulated ICAM-1 expression (IL-1 beta > TNF alpha > IFN-gamma >> PDGF-bb, IL-6), but not GM-CSF or TGF beta. A similar concentration-dependent increase was observed for synoviocytes derived from patients with rheumatoid or osteoarthritis. Kinetic studies of ICAM-1 expression differed among several cytokines: an early rise with IL-1 beta or TNF alpha stimulation, a gradual increase with IFN-gamma, a transient increase with PDGF-bb, and a plateau with IL-6. Adhesion of PBMC to synoviocytes was increased by IL-1 beta or TNF alpha and reduced by MAb to CD54 or CD18. Increased synoviocyte adhesiveness may promote interactions with infiltrating inflammatory cells.
我们测定了促炎细胞因子增强人滑膜细胞上细胞间黏附分子-1(ICAM-1,即CD54)表达以及外周血单个核细胞(PBMC)与滑膜细胞黏附的能力。通过细胞酶联免疫吸附测定法和流式细胞术对外表面分子进行了表征。通过直接计数或比色染色来测定PBMC与滑膜细胞单层的黏附情况。大多数细胞因子上调了ICAM-1的表达(白细胞介素-1β>肿瘤坏死因子α>γ干扰素>>血小板衍生生长因子-bb、白细胞介素-6),但粒细胞-巨噬细胞集落刺激因子或转化生长因子β未上调其表达。类风湿性关节炎或骨关节炎患者来源的滑膜细胞也观察到了类似的浓度依赖性增加。几种细胞因子之间ICAM-1表达的动力学研究结果有所不同:白细胞介素-1β或肿瘤坏死因子α刺激后早期升高,γ干扰素刺激后逐渐增加,血小板衍生生长因子-bb刺激后短暂增加,白细胞介素-6刺激后达到平台期。白细胞介素-1β或肿瘤坏死因子α增加了PBMC与滑膜细胞的黏附,而抗CD54或CD18单克隆抗体则降低了这种黏附。滑膜细胞黏附性增加可能会促进其与浸润性炎症细胞的相互作用。