Abnormal IgG galactosylation and arthritis in MRL‐Faslpr or MRL‐FasLgld mice are under the control of the MRL genetic background

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Abstract
MRL mice bearing the lpr (Fas) or gld (Fas ligand) mutation, MRL-Faslpr or MRL-FasLgld , respectively, develop arthritis similar to rheumatoid arthritis, but C3H and C57BL/6 mice bearing such mutations do not. In MRL-Faslpr 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-Faslpr and MRL-FasLgld mice. In contrast, the incidence of IgG without galactose was comparable among C3H-Faslpr , C3H-FasLgld , and C3H-+/+ mice as well as between C57BL/6-Faslpr and C57BL/6-+/+ mice. These results suggest that the increase in agalactosylated IgG and the development of arthritis in MRL-Faslpr and MRL-FasLgld mice are controlled by the MRL genetic background.