Hypercatabolism of IgG in mice with lupus-like syndrome

J. Zhou, L. M. Pop, Victor Ghetie

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The metabolism of radioiodinated mouse IgG was studied in mice with lupus-like syndrome before and after the onset of the disease. Before the onset of the disease, the pharmacokinetic parameters of IgG in MLR-lpr and Pristane-primed Balb/c mice were within the normal range of values. After the onset of the disease a considerable increase in the catabolic rate of IgG was recorded abbreviating its half life to less than one third of the normal value. The increased catabolism of IgG could not be related to the concentration- catabolism effect or to the presence of rheumatoid factor and autoantibody or to the IgG loss through the kidney and gastrointestinal tract. The hypercatabolism of IgG was explained by disease-induced impairment of the function of the receptor FcRn, which regulates the homeostasis of IgG.

Original languageEnglish (US)
Pages (from-to)458-466
Number of pages9
JournalLupus
Volume14
Issue number6
DOIs
StatePublished - Jul 21 2005

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Immunoglobulin G
Reference Values
Rheumatoid Factor
Autoantibodies
Half-Life
Gastrointestinal Tract
Homeostasis
Pharmacokinetics
Kidney

Keywords

  • Catabolism
  • IgG
  • Lupus
  • Mice

ASJC Scopus subject areas

  • Rheumatology

Cite this

Hypercatabolism of IgG in mice with lupus-like syndrome. / Zhou, J.; Pop, L. M.; Ghetie, Victor.

In: Lupus, Vol. 14, No. 6, 21.07.2005, p. 458-466.

Research output: Contribution to journalArticle

Zhou, J. ; Pop, L. M. ; Ghetie, Victor. / Hypercatabolism of IgG in mice with lupus-like syndrome. In: Lupus. 2005 ; Vol. 14, No. 6. pp. 458-466.
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