The neonatal Fc receptor as therapeutic target in IgG-mediated autoimmune diseases.

Therapy approaches based on lowering levels of pathogenic autoantibodies represent rational, effective, and safe treatment modalities of autoimmune diseases. The neonatal Fc receptor (FcRn) is a major factor regulating the serum levels of IgG antibodies. While FcRn-mediated half-life extension is beneficial for IgG antibody responses against pathogens, it also prolongs the serum half-life of IgG autoantibodies and thus promotes tissue damage in autoimmune diseases. In the present review article, we examine current evidence on the relevance of FcRn in maintaining high autoantibody levels and discuss FcRn-targeted therapeutic approaches. Further investigation of the FcRn-IgG interaction will not only provide mechanistic insights into the receptor function, but should also greatly facilitate the design of therapeutics combining optimal pharmacokinetic properties with the appropriate antibody effector functions in autoimmune diseases.
AuthorsAlina Sesarman, Gestur Vidarsson, Cassian Sitaru
JournalCellular and molecular life sciences : CMLS (Cell Mol Life Sci) Vol. 67 Issue 15 Pg. 2533-50 (Aug 2010) ISSN: 1420-9071 [Electronic] Switzerland
PMID20217455 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
Chemical References
  • Antibodies
  • Autoantibodies
  • Fc receptor, neonatal
  • Histocompatibility Antigens Class I
  • Immunoglobulin Fc Fragments
  • Receptors, Fc
  • Animals
  • Antibodies (blood, immunology, metabolism)
  • Autoantibodies (immunology)
  • Autoimmune Diseases (drug therapy, immunology, therapy)
  • Half-Life
  • Histocompatibility Antigens Class I
  • Immunoglobulin Fc Fragments (immunology)
  • Mice
  • Rats
  • Receptors, Fc (immunology, metabolism)
  • Serum (immunology, metabolism)

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