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.
Keywords: Genetic; Guillain–Barré syndrome; HLA; Polymorphism.