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

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.