ISOTYPE SWITCHING IN A NEOPLASTIC B CELL MODEL, BCL1

小鼠B细胞瘤BCL1表面既表达IgM又表达IgD 并可在体外被有丝分裂原诱导分泌更高水平的IgM。一个 已经开发出对BCDF有反应的肿瘤的非分泌性亚克隆 MU，一种存在于PK7.1T细胞上清液中的淋巴因子，通过增加其 Mu‘s m RNA转录及伴随的IgM分泌。这个亚克隆 目前正在作为BCDF伽马的目标细胞进行研究，另一个 淋巴因子存在于PK7.1上清液中。已经建立了条件 对于该因子与纯化的脾B细胞进行特异性诱导 Ig G1b和Ig G3的合成受到抑制。 BCL1品系的几个可能的开关变体已经被分离和 正在进行分子表征。主要目标是建立 T依赖同工型的精确重组机制和重组点 换个位置。(磅)

The murine B-cell tumor, BCL1, expresses both IgM and IgD on its surface and is inducible by mitogens to secrete greater levels of IgM in vitro. A nonsecreting subclone of the tumor has been developed that responds to BCDF mu, a lymphokine present in PK7.1 T-cell supernatants, by increasing its transcription of mu's mRNA and concomitant secretion of IgM. This subclone is currently being investigated as a target cell for BCDF gamma, another lymphokine present in PK7.1 supernatants. Conditions have been established for this factor with purified splenic B cells for specific induction of IgG1 message and protein while IgG2b and IgG3 synthesis is suppressed. Several putative switch variants of the BCL1 line have been isolated and are under molecular characterization. The principal goal is to establish the precise mechanism and point of recombination for a T-dependent isotype switch. (LB)