Abnormal IgG galactosylation and arthritis in MRL-Fas(lpr) or MRL-FasL(gld) mice are under the control of the MRL genetic background

Citation
Y. Kuroda et al., Abnormal IgG galactosylation and arthritis in MRL-Fas(lpr) or MRL-FasL(gld) mice are under the control of the MRL genetic background, FEBS LETTER, 507(2), 2001, pp. 210-214
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FEBS LETTERS
ISSN journal
0014-5793 → ACNP
Volume
507
Issue
2
Year of publication
2001
Pages
210 - 214
Database
ISI
SICI code
0014-5793(20011026)507:2<210:AIGAAI>2.0.ZU;2-N
Abstract
MRL mice bearing the lpr (Fas) or gld (Fas ligand) mutation, MRL-Fas(lpr) o r MRL-FasL(gld). respectively, develop arthritis similar to rheumatoid arth ritis, but C3H and C57BL/6 mice bearing such mutations do not. In MRL-Fas(l pr) mice, agalactosylated oligosaccharides in serum IgG increase significan tly in comparison to MRL-+/+ mice without arthritis. In this study, an incr eased level of agalactosylation in IgG, as compared to MRL-+/+, was found i n both MRL-Fas(lpr) and MRL-FasL(gld) mice. In contrast, the incidence of I gG 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. Thes e results suggest that the increase in agalactosylated IgG and the developm ent of arthritis in MRL-Fas(lpr) and MRL-FasL(gld) mice are controlled by t he MRL genetic background. (C) 2001 Federation of European Biochemical Soci eties. Published by Elsevier Science B.V. All rights reserved.