| First Author | Yamamoto N | Year | 1996 |
| Journal | Immunol Lett | Volume | 50 |
| Issue | 1-2 | Pages | 35-40 |
| PubMed ID | 8793557 | Mgi Jnum | J:34280 |
| Mgi Id | MGI:81743 | Doi | 10.1016/0165-2478(96)02514-x |
| Citation | Yamamoto N, et al. (1996) A defect in beta-galactosidase of B lymphocytes in the osteopetrotic (op/op) mouse. Immunol Lett 50(1-2):35-40 |
| abstractText | 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 D-3-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 lyse-Pc-inducible beta- galactosidase activity of B lymphocytes was found to be defective in op/op mouse. |
