Vachula M, Van Epps D E
Baxter Healthcare Corporation, Round Lake, Ill. 60073.
Invasion Metastasis. 1992;12(2):66-81.
The processes of lymphocyte-endothelial cell interaction and the in vitro assays employed in their study are the subjects of this review. In motility assays in porous filters and gel matrices, it has been shown that lymphocyte migration can be modulated by interleukin-2 (IL-2), IL-3, IL-4, IL-6, and IL-8. Cytokines can also modulate lymphocyte-endothelial adhesion. Endothelial intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) are induced or upregulated by IL-1 or tumor necrosis factor. In addition, interferon-gamma upregulates ICAM-1, and IL-4 can induce VCAM-1. The roles of these cytokines and adhesion molecules in transendothelial migration may be studied in assays in which lymphocytes penetrate layers of cultured endothelial cells. These models can distinguish lymphocyte adhesion from subsequent migration. Using such models, we and others have obtained evidence that both lymphocyte function-associated antigen-1 (LFA-1)/ICAM-1 and very late activation antigen 4 (VLA-4)/VCAM-1 interactions mediate lymphocyte adhesion to endothelial cells, but that LFA-1/ICAM-1 interactions play a greater role in transendothelial migration.
淋巴细胞与内皮细胞相互作用的过程以及用于其研究的体外检测方法是本综述的主题。在多孔滤器和凝胶基质中的迁移检测中，已表明淋巴细胞迁移可受到白细胞介素-2（IL-2）、IL-3、IL-4、IL-6和IL-8的调节。细胞因子也可调节淋巴细胞与内皮细胞的黏附。内皮细胞间黏附分子1（ICAM-1）和血管细胞黏附分子1（VCAM-1）可被IL-1或肿瘤坏死因子诱导或上调。此外，干扰素-γ上调ICAM-1，而IL-4可诱导VCAM-1。这些细胞因子和黏附分子在跨内皮迁移中的作用可在淋巴细胞穿透培养的内皮细胞层的检测中进行研究。这些模型可区分淋巴细胞黏附与随后的迁移。使用此类模型，我们和其他人已获得证据表明，淋巴细胞功能相关抗原-1（LFA-1）/ICAM-1和极晚期活化抗原4（VLA-4）/VCAM-1相互作用介导淋巴细胞与内皮细胞的黏附，但LFA-1/ICAM-1相互作用在跨内皮迁移中起更大作用。
