| Literature DB >> 33029737 |
Amin Safa1, Tahereh Azimi2, Arezou Sayad2, Mohammad Taheri3, Soudeh Ghafouri-Fard4.
Abstract
Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy syndrome. Several genetic and environmental risk factors have been recognized for GBS. AS GBS is an immune-related disorder, abnormal functions of T cells, production of autoantibodies, and dysregulation of gene expression have been detected in GBS patients. Based on the critical role of human leukocyte antigen (HLA) in the regulation of immune responses, HLA alleles are among the mostly investigated loci in GBS. A number of polymorphisms within different genes, especially those linked with the regulation of immune responses, have been associated with GBS in different populations. Moreover, several studies have demonstrated abnormal expression of cytokine-coding genes in this disorder. Investigations in the animal model of GBS have also verified the aberrant regulation of Th1/Th2/Th17/Treg cytokines. In the current review, we describe the information about the role of these factors in GBS.Entities:
Keywords: Genetic; Guillain–Barré syndrome; HLA; Polymorphism
Year: 2020 PMID: 33029737 DOI: 10.1007/s12031-020-01720-7
Source DB: PubMed Journal: J Mol Neurosci ISSN: 0895-8696 Impact factor: 3.444