大鼠自身免疫性周围神经炎症的多基因控制

Polygenic control of autoimmune peripheral nerve inflammation in rat.

作者信息

Dahlman I, Wallström E, Jiao H, Luthman H, Olsson T, Weissert R

机构信息

Neuroimmunology Unit, Center of Molecular Medicine, Karolinska Hospital, S-17176, Stockholm, Sweden.

出版信息

J Neuroimmunol. 2001 Oct 1;119(2):166-74. doi: 10.1016/s0165-5728(01)00395-2.

DOI:10.1016/s0165-5728(01)00395-2

PMID:11585618

Abstract

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.

摘要

实验性自身免疫性神经炎（EAN）是格林-巴利综合征（GBS）的主要动物模型，GBS是一种外周神经系统的炎症性疾病。对于这些疾病的基因调控了解甚少。我们首次对EAN进行了基因连锁分析。在一个大鼠F2群体中，EAN易感性与高水平的抗PNM IgG以及IgG2b和IgG2c同种型水平相关，这支持疾病基因调控Th1/Th2的优先分化。连锁分析表明EAN基因座与报道的实验性关节炎和/或脑脊髓炎的易感基因座以及17号染色体上的一个新区域共定位。对这些基因座的进一步剖析可能会揭示GBS中的疾病途径。