Identification of surface proteins mediating adherence of CD11/CD18-deficient lymphoblastoid cells to cultured human endothelium.
Identification of surface proteins mediating adherence of CD11/CD18-deficient lymphoblastoid cells to cultured human endothelium.
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介导 CD11/CD18 缺陷型淋巴母细胞与培养的人内皮细胞粘附的表面蛋白的鉴定。
DOI：
10.1172/jci114668
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Harlan,JM
中科院分区：
文献类型：
--
作者：
Schwartz,BR;Wayner,EA;Carlos,TM;Ochs,HD;Harlan,JM
患有严重白细胞粘附缺陷综合征的患者的任何白细胞上都不表达 CD11/CD18 粘附复合物。然而，与吞噬细胞不同，它们的淋巴细胞迁移到炎症的血管外部位，这表明除 CD11/CD18 之外的表面蛋白可以介导淋巴细胞与内皮的粘附。使用从 CD11/CD18 缺陷患者建立的 B 类淋巴母细胞系 (B-LCL) 和培养的人脐静脉内皮细胞 (HEC)，我们研究了淋巴细胞粘附内皮的 CD11/CD18 独立机制。针对淋巴细胞 VLA-4 整联蛋白受体 (CD49d/CD29) 的 α4 多肽 (CD49d) 和 β1 多肽 (CD29) 以及内皮细胞上的血管细胞粘附分子 1 (VCAM-1) 的单克隆抗体显着抑制 CD11/CD18 缺陷的 B-LCL 与未处理的 HEC 和经重组人肿瘤坏死处理的 HEC 的粘附因子-α。我们认为炎症或免疫反应部位细胞因子诱导的淋巴细胞受体 VLA-4 与内皮配体 VCAM-1 的相互作用代表了淋巴细胞迁移的 CD11/CD18 独立途径。
Patients with the severe form of leukocyte adhesion deficiency syndrome do not express the CD11/CD18 adhesion complex on any of their leukocytes. Nevertheless, their lymphocytes, unlike their phagocytes, emigrate to extravascular sites of inflammation, demonstrating that surface proteins other than CD11/CD18 can mediate lymphocyte adherence to endothelium. Using a B-lymphoblastoid cell line (B-LCL) established from a CD11/CD18-deficient patient and cultured human umbilical vein endothelial cells (HEC), we investigated the CD11/CD18-independent mechanism(s) of lymphocyte adherence to endothelium. Monoclonal antibodies directed to the alpha 4 polypeptide (CD49d) and the beta 1 polypeptide (CD29) of the lymphocyte VLA-4 integrin receptor (CD49d/CD29), and to vascular cell adhesion molecule-1 (VCAM-1) on the endothelial cell significantly inhibited the adherence of the CD11/CD18-deficient B-LCL to untreated HEC and to HEC treated with recombinant human tumor necrosis factor-alpha. We suggest that the interaction of the lymphocyte receptor VLA-4 with the endothelial ligand VCAM-1 induced by cytokines at sites of inflammation or immune reaction represents a CD11/CD18-independent pathway of lymphocyte emigration.