DISSECTION OF MURINE LYMPHOCYTE-ENDOTHELIAL CELL-INTERACTION MECHANISMS BY SV-40-TRANSFORMED MOUSE ENDOTHELIAL-CELL LINES - NOVEL MECHANISMS MEDIATING BASAL BINDING, AND ALPHA-4-INTEGRIN-DEPENDENT CYTOKINE-INDUCED ADHESION
DISSECTION OF MURINE LYMPHOCYTE-ENDOTHELIAL CELL-INTERACTION MECHANISMS BY SV-40-TRANSFORMED MOUSE ENDOTHELIAL-CELL LINES - NOVEL MECHANISMS MEDIATING BASAL BINDING, AND ALPHA-4-INTEGRIN-DEPENDENT CYTOKINE-INDUCED ADHESION
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DOI：
10.1016/0014-4827(91)90431-s
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发表时间：
1991-12-01
影响因子：
3.7
通讯作者：
HAMANN, A
中科院分区：
文献类型：
--
作者：
HARDER, R;UHLIG, H;HAMANN, A
淋巴结来源的内皮细胞通过SV40病毒感染永生化，并选择表达高内皮小静脉（HEV）特异性标记物meca325的亚克隆。这些转化的小鼠内皮（TME-）细胞系不需要特殊的生长因子就能永久生长。选择的克隆用内皮特异性抗体、抗血管性血友病因子抗血清和乙酰化低密度脂蛋白摄取染色，为其内皮起源提供了证据。单克隆抗体MECA 79和MECA 367在HEV上未检测到血管定位蛋白，表明HEV细胞的表型与HEV型内皮细胞的表型不同。TME细胞显示出与淋巴细胞结合的基本能力。用TNFα处理TME细胞可诱导另一种结合成分。针对已知阻断淋巴细胞与特定类型HEV相互作用的归巢受体LECAM-1（凝集素相关的白细胞内皮细胞粘附分子1）、α 4整合素、血管寻址蛋白、LFA-1或ICAM-1的抗体无法抑制对TME细胞的基础粘附，这表明该细胞类型在小鼠中显示了进一步的结合机制。TNFα诱导的粘附成分是由α 4整合素介导的，因为增强的结合可以被一种针对小鼠α 4（淋巴细胞- peyer 's斑块粘附分子12）的抗体阻断。因此，TME细胞系似乎是一个有用的模型，用于解剖和分析迄今为止尚未明确表征的小鼠淋巴细胞/内皮细胞相互作用机制。
Lymph node-derived endothelial cells were immortalized by infection with SV40 virus and subclones expressing the marker MECA 325 specific for high-endothelial venules (HEV) were selected. These transformed mouse endothelial (TME-) cell lines grow permanently without requirement for special growth factors. Staining of the selected clones with endothelium-speciflc antibodies and with anti-von Willebrand factor antiserum and uptake of acetylated low-density lipoprotein provide evidence for their endothelial origin. The vascular addressins identified by mAbs MECA 79 and MECA 367 on HEV are not detectable, indicating that the phenotype of the cells differs from that of HEV-type endothelium. The TME cells display a constitutive capacity to bind lymphocytes. An additional binding component is induced by treatment of the TME cells with TNFα. Antibodies against the homing receptor LECAM-1 (lectin-related leucocyte-endothelial cell adhesion molecule 1), α 4-integrins, vascular addressins, LFA-1, or ICAM-1 known to block lymphocyte interaction with particular types of HEV were unable to inhibit the basal adhesion to TME cells, indicating that a further binding mechanism in mice is displayed by this cell type. The adhesion component induced by TNFα is mediated by α 4-integrins since enhanced binding could be blocked by an antibody against mouse α 4 (lymphocyte-Peyer's patch adhesion molecule 1 2). TME cell lines therefore seem to be a useful model for the dissection and analysis of hitherto poorly characterized murine lymphocyte/endothelial cell interaction mechanisms.