骨石化（mi/mi）小鼠B淋巴细胞中诱导型β-半乳糖苷酶的缺陷。

A defect in inducible beta-galactosidase of B lymphocytes in the osteopetrotic (mi/mi) mouse.

作者信息

Yamamoto N, Naraparaju V R

机构信息

Laboratory of Cancer Immunology and Molecular Biology, Albert Einstein Cancer Center, Philadelphia, PA 19141, USA.

出版信息

Immunology. 1996 Aug;88(4):604-10. doi: 10.1046/j.1365-2567.1996.d01-684.x.

DOI:10.1046/j.1365-2567.1996.d01-684.x

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1456628/

Abstract

Macrophages were activated by administration of an inflammatory lipid metabolite, lysophosphatidylcholine (lyso-Pc), to wild type mice but not murine (microphthalmic) osteopetrotic (mi/mi) mutant mice. In vitro treatment of wild type mouse peritoneal cells with lyso-Pc efficiently activated macrophages whereas lyso-Pc-treatment of mi mutant mouse peritoneal cells resulted in no activation of macrophages. Generation of macrophage activating factor requires a precursor protein, serum vitamin D binding protein (DBP), and participation of lyso-Pc-inducible beta-galactosidase of B lymphocytes. Lyso-Pc-inducible beta-galactosidase of B lymphocytes was found to be defective in mi mutant mice.

摘要

通过向野生型小鼠注射炎性脂质代谢产物溶血磷脂酰胆碱（lyso-Pc）可激活巨噬细胞，但对小鼠（小眼症）骨石化（mi/mi）突变小鼠无效。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mi突变小鼠腹膜细胞则不会激活巨噬细胞。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D结合蛋白（DBP），以及B淋巴细胞中lyso-Pc诱导的β-半乳糖苷酶的参与。发现mi突变小鼠中B淋巴细胞的lyso-Pc诱导β-半乳糖苷酶存在缺陷。

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Immunol Lett. 1996 Apr;50(1-2):35-40. doi: 10.1016/0165-2478(96)02514-x.

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