Gld and lpr mice: single gene mutant models for failed self tolerance.
Mice homozygous for the gld or lpr mutations develop autoimmunity, and a lymphoproliferative disorder involving accumulation of huge numbers of unusual CD4-CD8-TCR alpha beta lo T cells. Here we review our past work with gld mice, and attempt to explain lymphoproliferation in terms of current models of T cell maturation and self-tolerance induction. The availability of molecular probes to the gene products of lpr and gld should shortly lead to a better understanding of the acquisition of self tolerance during T cell maturation and of autoimmunity.
Bhandoola
A
A
Department of Pathology, University of Pennsylvania Medical School, Philadelphia.
Yui
K
K
Siegel
R M
RM
Zerva
L
L
Greene
M I
MI
D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics* / Q000276:immunology; D008198:Lymph Nodes / Q000276:immunology; D008232:Lymphoproliferative Disorders / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008817:Mice, Mutant Strains / Q000235:genetics / Q000276:immunology*; D008822:Mice, Transgenic; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D017634:Self Tolerance / Q000235:genetics* / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013950:Thymus Gland / Q000276:immunology
D011948:Receptors, Antigen, T-Cell