Horsburgh C R, Clark R A, Kirkpatrick C H
J Leukoc Biol. 1987 Jan;41(1):14-24. doi: 10.1002/jlb.41.1.14.
Monocytes must accumulate in areas of tissue injury and inflammation to effect phagocytosis, antigen presentation, and monokine production. Fibrinogen/fibronectin matrices have been demonstrated in healing wounds and in delayed-type hypersensitivity skin reactions. We have developed an in vitro system for investigation of the ability of fibrinogen and fibronectin matrices to serve as substrata for human peripheral blood monocyte adherence. Monocyte adherence was greatest on matrices of both fibrinogen and fibronectin, less to fibrinogen alone, and least to fibronectin alone. Lymphokines increased adherence of monocytes to all three surfaces but not to albumin-coated surfaces. Addition of platelets also caused a dose-dependent increase in monocyte adherence to all three surfaces. This increased adherence was not a simple function of arachidonic acid metabolites, stable platelet products, nor monocyte binding sites on the platelet membrane. The effect of platelets was not additive to the effect of lymphokines. We conclude that fibrinogen and fibronectin provide a framework for monocyte adherence and that factors present in areas of inflammation and wound healing, such as lymphokines and platelets, can augment this adherence. Such adherence facilitates the transformation of monocytes into macrophages in vitro and may also foster such transformation in vivo.
单核细胞必须在组织损伤和炎症区域积聚，以实现吞噬作用、抗原呈递和单核因子产生。在愈合伤口和迟发型超敏皮肤反应中已证实存在纤维蛋白原/纤连蛋白基质。我们开发了一种体外系统，用于研究纤维蛋白原和纤连蛋白基质作为人外周血单核细胞黏附底物的能力。单核细胞在纤维蛋白原和纤连蛋白的基质上黏附性最强，仅在纤维蛋白原上的黏附性次之，仅在纤连蛋白上的黏附性最弱。淋巴因子增加了单核细胞在所有这三种表面上的黏附，但对白蛋白包被的表面没有影响。添加血小板也导致单核细胞在所有这三种表面上的黏附呈剂量依赖性增加。这种增加的黏附不是花生四烯酸代谢产物、稳定的血小板产物或血小板膜上单核细胞结合位点的简单作用。血小板的作用与淋巴因子的作用不是相加的。我们得出结论，纤维蛋白原和纤连蛋白为单核细胞黏附提供了一个框架，并且炎症和伤口愈合区域中存在的因子，如淋巴因子和血小板，可以增强这种黏附。这种黏附有助于体外单核细胞向巨噬细胞的转化，也可能促进体内的这种转化。
