Polygenic control of autoimmune peripheral nerve inflammation in rat.
Experimental autoimmune neuritis (EAN) is the principal animal model for Guillain-Barré syndrome (GBS), an inflammatory disease of the peripheral nervous system. Little is known on the genetic regulation of these diseases. We provide the first genetic linkage analysis of EAN. Susceptibility to EAN in a rat F2 population segregated with high levels of anti-PNM IgG, as well as IgG2b and IgG2c isotype levels, which support that disease genes regulate preferential Th1/Th2 differentiation. Linkage analysis demonstrated co-localization of EAN loci with reported susceptibility loci for experimental arthritis and/or encephalomyelitis and a new region on chromosome 17. Further dissection of these loci may disclose disease pathways in GBS.
Dahlman
I
I
Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S-17176, Stockholm, Sweden.
Wallström
E
E
Jiao
H
H
Luthman
H
H
Olsson
T
T
Weissert
R
R
D000818:Animals; D002875:Chromosomes; D004195:Disease Models, Animal; D005260:Female; D008040:Genetic Linkage; D005838:Genotype; D007074:Immunoglobulin G / Q000276:immunology; D008297:Male; D009444:Neuritis, Autoimmune, Experimental / Q000235:genetics* / Q000276:immunology*; D017933:Peripheral Nervous System / Q000276:immunology; D051381:Rats; D011912:Rats, Inbred ACI; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D007074:Immunoglobulin G