Yamamoto N, Naraparaju V R
Laboratory of Cancer Immunology and Molecular Biology, Albert Einstein Cancer Center, Philadglphia, PA 19141, USA.
Immunol Lett. 1996 Apr;50(1-2):35-40. doi: 10.1016/0165-2478(96)02514-x.
Macrophages were activated by administration of an inflammatory lipid metabolite, lysophosphatidylcholine (lyso-Pc), to wild type mice but not osteopetrotic op/op mice. In vitro treatment of wild type mouse peritoneal cells with lyso-Pc efficiently activated macrophages whereas lyso-Pc-treatment of op/op mouse peritoneal cells resulted in no significant activation of macrophages. Generation of macrophage activating factor requires a precursor protein, serum vitamin D3-binding protein (DBP), as well as participation of beta-galactosidase of lyso-Pc-primed B lymphocytes. The treatment of wild type mouse peritoneal cells with lyso-Pc induced beta-galactosidase of B lymphocytes leading to the conversion of DBP to macrophage activating factor and subsequent activation of macrophages. The lyso-Pc-inducible beta-galactosidase activity of B lymphocytes was found to be defective in op/op mouse.
通过向野生型小鼠而非骨质石化的op/op小鼠施用炎性脂质代谢物溶血磷脂酰胆碱（lyso-Pc）来激活巨噬细胞。用lyso-Pc体外处理野生型小鼠腹膜细胞可有效激活巨噬细胞，而用lyso-Pc处理op/op小鼠腹膜细胞则不会导致巨噬细胞的显著激活。巨噬细胞激活因子的产生需要一种前体蛋白，即血清维生素D3结合蛋白（DBP），以及lyso-Pc致敏的B淋巴细胞的β-半乳糖苷酶的参与。用lyso-Pc处理野生型小鼠腹膜细胞可诱导B淋巴细胞的β-半乳糖苷酶，导致DBP转化为巨噬细胞激活因子并随后激活巨噬细胞。发现op/op小鼠中B淋巴细胞的lyso-Pc诱导型β-半乳糖苷酶活性存在缺陷。
