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。