Radomska H S, Shen C P, Kadesch T, Eckhardt L A
Department of Biological Sciences, Hunter College, City University of New York, New York 10021, USA.
Immunity. 1994 Nov;1(8):623-34. doi: 10.1016/1074-7613(94)90034-5.
Recent experiments involving disruption of the Oct-2 gene have shown that this largely B cell-restricted transcription factor is not required in the early stages of B cell development. However, B cells that lack Oct-2 may be blocked from differentiation past the surface immunoglobulin-positive stage. To identify a possible function for Oct-2 in the late stage immunoglobulin-secreting cell, we have used the method of somatic cell fusion. When the immunoglobulin-producing myeloma MPC11 is fused to a T lymphoma, Oct-2 production ceases, as does the expression of immunoglobulin, J chain, and several other B cell-specific gene products. In the present study, we show that by preventing the loss of Oct-2 in the hybrid cells, we can preserve expression of all other tested B cell-specific genes. These results establish a central role for Oct-2 in maintaining the genetic program of the immunoglobulin-secreting plasmacyte.
最近涉及Oct-2基因破坏的实验表明，这种主要在B细胞中受限的转录因子在B细胞发育的早期阶段并非必需。然而，缺乏Oct-2的B细胞可能在分化过程中受阻于表面免疫球蛋白阳性阶段之后。为了确定Oct-2在晚期免疫球蛋白分泌细胞中的可能功能，我们采用了体细胞融合方法。当产生免疫球蛋白的骨髓瘤MPC11与T淋巴瘤融合时，Oct-2的产生停止，免疫球蛋白、J链和其他几种B细胞特异性基因产物的表达也随之停止。在本研究中，我们表明通过防止杂交细胞中Oct-2的丢失，我们可以保留所有其他测试的B细胞特异性基因的表达。这些结果确立了Oct-2在维持免疫球蛋白分泌浆细胞的遗传程序中的核心作用。
