NOVAL HUMAN MACROPHAGE RECEPTOR

我们已经使用选择性配体cgp 42112来调节新的 本课题组描述的人类巨噬细胞-小胶质细胞受体 单核/巨噬细胞和大鼠脑内病变。我们发现 CGp 42112拮抗卡介苗对巨噬细胞的刺激作用 脂多糖抑制细胞因子和金属蛋白ASE-g 由人类巨噬细胞产生。这些结果可能表明CGP 42112及相关化合物可具有抗免疫、抗炎作用 属性。 我们还发现Cgp 42 112结合位点在 球囊插管动脉的外膜，提示这些 动脉损伤炎症反应中的受体。在大鼠体内 脑、生理和化学损伤导致CGp 42112的表达 受体，这与神经元死亡有关，在这两个部位 病变远端，反映病变的退行性变 投射的神经末梢。我们建议CGP42112扮演一个角色 受体在神经元损伤和修复机制中的作用。 我们继续努力克隆新的巨噬细胞/小胶质细胞受体 从人单核细胞和大鼠脾的cdna文库中提取。

We have used the selective ligand CGP 42112 to modulate the novel macrophage-microglial receptor described by our group in human monocytes/macrophages and in lesions of the rat brain. We found that CGP 42112 antagonizes the macrophage stimulation produced by lipopolysacharide, inhibiting the cytokine and metalloprotein ase-g production by human macrophages. These results may suggest that CGP 42112 and related compounds can have anti-immune, anti-inflammatory properties. We have also showed that CGP 42 112 binding sites are expressed in the adventitia of balloon-catheterized arteries, suggesting a role for these receptors in the inflammatory reaction to arterial injury. In the rat brain, physical and chemical lesions result in expression of CGP 42112 receptors, and this is associated with neuronal death, both at the site of the lesion and distal to the lesion, reflecting degeneration of projecting neuronal terminals. We suggest a role for CGP 42112 receptors in the mechanisms of neuronal injury and repair. We continue our efforts to clone the novel macrophage/microglia receptor from a cDNA library from human monocytes and rat spleen.