Leukocyte adhesion molecule-1 (LAM-1, L-selectin) interacts with an inducible endothelial cell ligand to support leukocyte adhesion.
Leukocyte adhesion molecule-1 (LAM-1, L-selectin) interacts with an inducible endothelial cell ligand to support leukocyte adhesion.
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DOI：
10.4049/jimmunol.147.8.2565
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发表时间：
1991-10
影响因子：
4.4
通讯作者：
O. Spertini;F. Luscinskas;G. Kansas;J. Munro;James D. Griffin;M. Gimbrone;T. Tedder
中科院分区：
文献类型：
--
作者：
O. Spertini;F. Luscinskas;G. Kansas;J. Munro;James D. Griffin;M. Gimbrone;T. Tedder
人淋巴细胞归巢受体LAM-1介导淋巴细胞粘附于外周淋巴结的特化高内皮微静脉（HEV）。我们现在报道LAM-1也是白细胞附着于活化的人内皮的主要介质。在一种新的粘附试验中，LAM-1显示在4 ℃下介导淋巴细胞和中性粒细胞与TNF活化的人脐静脉内皮细胞的粘附的约50%。只有在旋转（非静态）条件下进行试验时，才能检测到LAM-1对白细胞粘附的贡献，这表明LAM-1参与了白细胞与内皮细胞的初始粘附。在37 ℃的该试验中，基本上所有淋巴细胞与内皮的附着都是由LAM-1、VLA-4/VCAM-1和CD 11/CD 18复合物介导的，而中性粒细胞附着是由LAM-1、内皮-白细胞粘附分子-1和CD 11/CD 18介导的。因此，多种受体是必要的，以促进最佳的白细胞粘附到内皮。LAM-1似乎也参与了最佳的中性粒细胞跨内皮迁移使用的视频显微镜在体外transmigration模型系统。LAM-1依赖性白细胞粘附需要神经氨酸酶敏感分子的诱导和表面表达，所述神经氨酸酶敏感分子在活化的内皮上表达至少24小时。内皮细胞的LAM-1配体的表达最佳地由LPS和促炎细胞因子TNF-α和IL-1 β诱导，而IFN-γ和IL-4诱导较低水平的表达。HEV和细胞因子处理的内皮上的LAM-1配体可能是类似的含碳水化合物的分子，因为来自酵母汉逊酵母细胞壁的磷酸甘露聚糖单酯核心复合物阻断淋巴细胞与两种细胞类型的结合，并且LAM-1介导的淋巴细胞附着到HEV和活化的内皮上的表位相同。因此，LAM-1和它的可诱导的内皮配体构成了一对新的粘附分子，可以调节炎症部位的初始白细胞/内皮相互作用。
The human lymphocyte homing receptor, LAM-1, mediates the adhesion of lymphocytes to specialized high endothelial venules (HEV) of peripheral lymph nodes. We now report that LAM-1 is also a major mediator of leukocyte attachment to activated human endothelium. In a novel adhesion assay, LAM-1 was shown to mediate approximately 50% of the adhesion of both lymphocytes and neutrophils to TNF-activated human umbilical vein endothelial cells at 4 degrees C. The contribution of LAM-1 to leukocyte adhesion was only detectable when the assays were carried out under rotating (nonstatic) conditions, suggesting that LAM-1 is involved in the initial attachment of leukocytes to endothelium. In this assay at 37 degrees C, essentially all lymphocyte attachment to endothelium was mediated by LAM-1, VLA-4/VCAM-1, and the CD11/CD18 complex, whereas neutrophil attachment was mediated by LAM-1, endothelial-leukocyte adhesion molecule-1, and CD11/CD18. Thus, multiple receptors are necessary to promote optimal leukocyte adhesion to endothelium. LAM-1 also appeared to be involved in optimal neutrophil transendothelial migration using a videomicroscopic in vitro transmigration model system. LAM-1-dependent leukocyte adhesion required the induction and surface expression of a neuraminidase-sensitive molecule that was expressed for at least 24 h on activated endothelium. Expression of the LAM-1 ligand by endothelium was optimally induced by LPS and the proinflammatory cytokines TNF-alpha and IL-1 beta, whereas IFN-gamma and IL-4 induced lower levels of expression. The LAM-1 ligand on HEV and cytokine treated endothelium may be similar carbohydrate-containing molecules, because phosphomannan monoester core complex from yeast Hansenula hostii cell wall blocked binding of lymphocytes to both cell types, and identical epitopes on LAM-1-mediated lymphocyte attachment to HEV and activated endothelium. Thus, LAM-1 and its inducible endothelial ligand constitute a new pair of adhesion molecules that may regulate initial leukocyte/endothelial interactions at sites of inflammation.