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

Yasuhiro Kuroda, Munehiro Nakata, Masato Nose, Naoya Kojima, Tsuguo Mizuochi

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)210-214
Number of pages5
JournalFEBS Letters
Volume507
Issue number2
DOIs
Publication statusPublished - 2001 Oct 26

Keywords

  • Apoptosis
  • Arthritis
  • Glycosylation
  • IgG
  • gld
  • lpr

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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