Aggregation of macrophages and fibroblasts is inhibited by a monoclonal antibody to the hyaluronate receptor.
Aggregation of macrophages and fibroblasts is inhibited by a monoclonal antibody to the hyaluronate receptor.
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透明质酸受体的单克隆抗体可抑制巨噬细胞和成纤维细胞的聚集。
DOI：
10.1016/0014-4827(88)90393-x
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发表时间：
1988
影响因子：
3.7
通讯作者：
Underhill,CB
中科院分区：
文献类型：
--
作者：
Green,SJ;Tarone,G;Underhill,CB
为了研究透明质酸受体在细胞间粘附中的作用，我们使用了K-3单克隆抗体（MAb），该抗体特异性地结合透明质酸受体并阻断其与透明质酸相互作用的能力。在第一组实验中，我们研究了SV-3T3细胞的自发聚集，其中涉及两种不同的机制，其中一种依赖于二价阳离子的存在，另一种是独立的。发现K-3单抗的完整片段和Fab片段完全抑制了二价阳离子非依赖性聚集。相比之下，K-3单抗对细胞的二价阳离子依赖性聚集没有影响。在第二组实验中，我们检测了肺泡巨噬细胞。肺泡巨噬细胞上存在透明质酸受体，这些细胞的洗涤剂提取物可以结合[3H]透明质酸，这种结合被K-3单抗阻断。肺泡巨噬细胞免疫印迹分析显示，透明质酸受体的M值为99,500，明显大于BHK细胞的85,000。将透明质酸加入肺泡巨噬细胞悬浮液中，诱导细胞聚集。这种作用被K-3单抗抑制，表明透明质酸诱导的聚集是由受体介导的。
To examine the role of the hyaluronate receptor in cell to cell adhesion, we have employed the K-3 monoclonal antibody (MAb) which specifically binds to the hyaluronate receptor and blocks its ability to interact with hyaluronate. In the first set of experiments, we investigated the spontaneous aggregation of SV-3T3 cells, which involves two distinct mechanisms, one of which is dependent upon the presence of divalent cation and the other is independent. The divalent cation-independent aggregation was found to be completely inhibited by both intact and Fab fragments of the K-3 MAb. In contrast, the K-3 MAb had no effect on the divalent cation-dependent aggregation of cells. In a second set of experiments, we examined alveolar macrophages. The presence of hyaluronate receptors on alveolar macrophages was demonstrated by the fact that detergent extracts of these cells could bind [3H]hyaluronate, and this binding was blocked by the K-3 MAb. Immunoblot analysis of alveolar macrophages showed that the hyaluronate receptor had a M, of 99,500, which is considerably larger than the 85,000Mrfor that on BHK cells. When hyaluronate was added to suspensions of alveolar macrophages, the cells were induced to aggregate. This effect was inhibited by the K-3 MAb, suggesting that the hyaluronate-induced aggregation was mediated by the receptor.