Fc gamma receptors in the initiation and progression of systemic lupus erythematosus

E Reefman*, HM Dijstelbloem, PC Limburg, CGM Kallenberg, M Bijl

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

18 Citations (Scopus)

Abstract

Systemic lupus erythematosus, a systemic autoimmune disorder, is characterized by the production of autoantibodies to nuclear constituents and inflammatory lesions in multiple organ systems. Although the pathogenesis of the disease is largely unknown, recent studies have suggested that disturbances in apoptosis and/or clearance of apoptotic cells may play an important role in the induction and perpetuation of autoantibody production. When autoantibodies subsequently complex to autoantigens present on apoptotic cells, ligation of Fcgamma receptor will result in inflammation and disease development. Indeed, mice deficient in activating Fcgamma receptors were protected against inflammation in models of immune complex-mediated autoimmune disease, whereas deletion of the inhibitory Fcgamma receptors increased autoantibody production and susceptibility to immune complex-induced inflammation. Additionally, functional polymorphisms in Fcgamma receptors were shown to be associated with development of human systemic lupus erythematosus. This review focuses on the role of Fcgamma receptors in the initiation of autoantibody production, inflammatory handling of immune complexes, and disease development in systemic lupus erythematosus.

Original languageEnglish
Pages (from-to)382-389
Number of pages8
JournalImmunology and Cell Biology
Volume81
Issue number5
Publication statusPublished - Oct-2003

Keywords

  • autoimmunity
  • Fc gamma receptors
  • systemic lupus erythematosus
  • MONOCYTE-DERIVED MACROPHAGES
  • COLLAGEN-INDUCED ARTHRITIS
  • APOPTOTIC CELLS
  • DEFICIENT MICE
  • AUTOIMMUNE-DISEASE
  • GENETIC SUSCEPTIBILITY
  • IIA POLYMORPHISM
  • KOREAN PATIENTS
  • RIIA ALLELES
  • RISK FACTOR

Cite this