The lpr and gld genes in systemic autoimmunity: life and death in the Fas lane

Immunol Today. 1992 Nov;13(11):427-8. doi: 10.1016/0167-5699(92)90066-G.

Abstract

The single gene lpr and gld models of spontaneous systemic autoimmunity have attracted much attention in recent years. Here, Philip Cohen and Robert Eisenberg describe the fascinating recent findings that the lpr and gld [corrected] phenotypes result from defects in the Fas gene and, perhaps, in the ligand for fas, respectively.

Publication types

  • Review

MeSH terms

  • Animals
  • Antigens, Surface / genetics
  • Antigens, Surface / physiology*
  • Apoptosis / genetics*
  • Autoimmune Diseases / genetics*
  • Autoimmunity / genetics*
  • B-Lymphocytes / immunology
  • B-Lymphocytes / pathology
  • Disease Models, Animal*
  • Genes*
  • Immune Tolerance / genetics
  • Ligands
  • Lupus Erythematosus, Systemic / genetics*
  • Lymphoproliferative Disorders / genetics*
  • Membrane Proteins / genetics
  • Membrane Proteins / physiology*
  • Mice
  • Mice, Mutant Strains / genetics
  • Mice, Mutant Strains / immunology*
  • Phenotype
  • Radiation Chimera
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / pathology
  • Thymus Gland / pathology
  • fas Receptor

Substances

  • Antigens, Surface
  • Ligands
  • Membrane Proteins
  • fas Receptor