Experimental autoimmune neuritis (EAN) is the principal animal model for Gu
illain-Barre syndrome (GBS), an inflammatory disease of the peripheral nerv
ous system. Little is known on the genetic regulation of these diseases. We
provide the first genetic linkage analysis of EAN. Susceptibility to EAN i
n 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 regulat
e preferential Th1/Th2 differentiation. Linkage analysis demonstrated co-lo
calization of EAN loci with reported susceptibility loci for experimental a
rthritis and/or encephalomyelitis and a new region on chromosome 17, Furthe
r dissection of these loci may disclose disease pathways in GBS. (C) 2001 E
lsevier Science B.V. All rights reserved.