Abnormal IgG galactosylation and arthritis in MRL-Fas(lpr) or MRL-FasL(gld) mice are under the control of the MRL genetic background.
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.
Kuroda
Y
Y
Department of Applied Biochemistry, Tokai University, Hiratsuka, Kanagawa, Japan.
Nakata
M
M
Nose
M
M
Kojima
N
N
Mizuochi
T
T
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000235:genetics / Q000378:metabolism*; D002240:Carbohydrate Sequence; D053222:Fas Ligand Protein; D005690:Galactose / Q000378:metabolism*; D007074:Immunoglobulin G / Q000378:metabolism*; D008562:Membrane Glycoproteins / Q000235:genetics*; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr / Q000235:genetics*; D008969:Molecular Sequence Data; D009844:Oligosaccharides / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics*
D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D007074:Immunoglobulin G; D008562:Membrane Glycoproteins; D009844:Oligosaccharides; C064155:agalactosyl IGG; D019014:fas Receptor; D005690:Galactose