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两种小鼠浆细胞瘤细胞培养适应株中免疫球蛋白表型的改变。

Alteration of immunoglobulin phenotype in cell culture-adapted lines of two mouse plasmacytomas.

作者信息

Hausman S J, Bosma M J

出版信息

J Exp Med. 1975 Oct 1;142(4):998-1010. doi: 10.1084/jem.142.4.998.

Abstract

Murine plasmacytomas can be adapted to continuous in vitro culture by alternate passage between culture and animal. We have found that the kinetics of adaptation reflect a selection for the growth of variant plasmacytoma cells. The inclusion of an altered immunoglobulin phenotype in such variant cells could explain the Ig-producing variants that we observed in two of six transplantable lines of plasmacytomas that were adapted to culture. The first variant, an IgM-producing cell line (104-76), was adapted from a transplanted line of MOPC 104E that had stopped producing IgM with binding specificity for alpha1-3 Dextran. Unlike MOPC 104E, the IgM of 104-76 contains kappa- instead of lambda-light chains and probably contains an altered or different mu-heavy chain. A second variant (352-57) was found in an IgG2b-producing tumor (MOPC 352) which was induced in a BALB/c mouse strain (CB-6) that carried Ig genes of the C57BL/Ka allotype. This cell line apparently switched from producing IgG2b molecules of the C57BL allotype (H9) and of a known idiotype to IgG1 molecules of the BALB/c allotype (F19) without the idiotype marker. The propagation of a biclonal plasmacytoma from the time of original tumor induction does not appear as a likely explanation for these results. Rather, we seem to be dealing with plasmacytoma variants or with the possible induction of secondary tumors of host origin.

摘要

鼠浆细胞瘤可通过在培养物和动物之间交替传代来适应连续的体外培养。我们发现,适应的动力学反映了对浆细胞瘤变异细胞生长的选择。在这些变异细胞中包含改变的免疫球蛋白表型可以解释我们在六个适应培养的可移植浆细胞瘤系中的两个中观察到的产生Ig的变异体。第一个变异体是一个产生IgM的细胞系(104-76),它是从已停止产生对α1-3葡聚糖具有结合特异性的IgM的MOPC 104E移植系改编而来。与MOPC 104E不同,104-76的IgM含有κ链而非λ链,并且可能含有改变的或不同的μ重链。在一个产生IgG2b的肿瘤(MOPC 352)中发现了第二个变异体(352-57),该肿瘤是在携带C57BL/Ka同种异型Ig基因的BALB/c小鼠品系(CB-6)中诱导产生的。这个细胞系显然从产生C57BL同种异型(H9)和已知独特型的IgG2b分子转变为产生没有独特型标记的BALB/c同种异型(F19)的IgG1分子。从原始肿瘤诱导时起双克隆浆细胞瘤的增殖似乎不是这些结果的可能解释。相反,我们似乎在处理浆细胞瘤变异体或宿主来源的继发性肿瘤的可能诱导。

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