抄録
We previously demonstrated that treatment of human gingival fibroblasts (GF) with anti-CD 44 mAb (OS/37) enhanced the adhesion between K 562 (erythroleukemia line) and GF and that anti-CD 43 mAb, 3 S-B 2, specifically inhibited this heterotypic cell adhesion. In this study, the regulatory mechanism of GF-K 562 interaction by 3 S-B 2 was investigated. In order to assess the possibility that CD 43 may function as an adhesion molecule between GF and K 562, soluble chimeric CD 43, CD 43-Ig, was added to the co-culture of K 562 and OS/37-treated GF. However, CD 43-Ig did not inhibit the heterotypic cell adhesion. This suggests that CD 43 on K 562 may not be directly involved in the adhesion to OS/37-treated GF. We then examined the possible regulatory mechanism via CD 43-cytoplasmic domain in this heterotypic cell adhesion. By transfecting full length or cytoplasmic region- deleted human CD 43 cDNA into mouse thymoma (EL-4), we established EL-4-CD 43 F or EL-4-CD 43 TM, respectively. Although these two transfectants expressed equal level of exogenous CD 43 molecules, 3 S-B 2 inhibited the binding between OS/37-treated GF and EL-4-CD 43 F, but not EL-4-CD 43 TM. These results demonstrate that acting as a signal transducing molecule, CD 43 regulates the GF-K 562 binding probably via a cytoplasmic domain of CD 43.
