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MRL-Fas(lpr)或MRL-FasL(gld)小鼠中异常的IgG半乳糖基化和关节炎受MRL遗传背景的控制。

Abnormal IgG galactosylation and arthritis in MRL-Fas(lpr) or MRL-FasL(gld) mice are under the control of the MRL genetic background.

作者信息

Kuroda Y, Nakata M, Nose M, Kojima N, Mizuochi T

机构信息

Department of Applied Biochemistry, Tokai University, Hiratsuka, Kanagawa, Japan.

出版信息

FEBS Lett. 2001 Oct 26;507(2):210-4. doi: 10.1016/s0014-5793(01)02974-x.

DOI:10.1016/s0014-5793(01)02974-x
PMID:11684100
Abstract

MRL mice bearing the lpr (Fas) or gld (Fas ligand) mutation, MRL-Fas(lpr) or MRL-FasL(gld), respectively, develop arthritis similar to rheumatoid arthritis, but C3H and C57BL/6 mice bearing such mutations do not. In MRL-Fas(lpr) mice, agalactosylated oligosaccharides in serum IgG increase significantly in comparison to MRL-+/+ mice without arthritis. In this study, an increased level of agalactosylation in IgG, as compared to MRL-+/+, was found in both MRL-Fas(lpr) and MRL-FasL(gld) mice. In contrast, the incidence of IgG without galactose was comparable among C3H-Fas(lpr), C3H-FasL(gld), and C3H-+/+ mice as well as between C57BL/6-Fas(lpr) and C57BL/6-+/+ mice. These results suggest that the increase in agalactosylated IgG and the development of arthritis in MRL-Fas(lpr) and MRL-FasL(gld) mice are controlled by the MRL genetic background.

摘要

分别携带lpr(Fas)或gld(Fas配体)突变的MRL小鼠,即MRL-Fas(lpr)或MRL-FasL(gld),会发展出类似于类风湿性关节炎的关节炎,但携带此类突变的C3H和C57BL/6小鼠则不会。与没有关节炎的MRL-+/+小鼠相比,MRL-Fas(lpr)小鼠血清IgG中的去半乳糖基化寡糖显著增加。在本研究中,与MRL-+/+相比,在MRL-Fas(lpr)和MRL-FasL(gld)小鼠中均发现IgG的去半乳糖基化水平升高。相比之下,在C3H-Fas(lpr)、C3H-FasL(gld)和C3H-+/+小鼠之间以及C57BL/6-Fas(lpr)和C57BL/6-+/+小鼠之间,不含半乳糖的IgG发生率相当。这些结果表明,MRL-Fas(lpr)和MRL-FasL(gld)小鼠中去半乳糖基化IgG的增加以及关节炎的发展受MRL遗传背景的控制。

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