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Abnormal IgG galactosylation and arthritis in MRL‐ Fas lpr or MRL‐ FasL gld mice are under the control of the MRL genetic background
Author(s) -
Kuroda Yasuhiro,
Nakata Munehiro,
Nose Masato,
Kojima Naoya,
Mizuochi Tsuguo
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)02974-x
Subject(s) - fas ligand , rheumatoid arthritis , arthritis , medicine , immunology , endocrinology , apoptosis , chemistry , biochemistry , programmed cell death
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.