A review of the role of genetic factors in Guillain-Barré syndrome.
Amin SafaTahereh AzimiArezou SayadMohammad TaheriSoudeh Ghafouri-FardPublished in: Journal of molecular neuroscience : MN (2020)
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.
Keyphrases
- genome wide
- immune response
- gene expression
- risk factors
- end stage renal disease
- dna methylation
- case report
- ejection fraction
- systemic lupus erythematosus
- chronic kidney disease
- poor prognosis
- liver failure
- oxidative stress
- toll like receptor
- healthcare
- peritoneal dialysis
- copy number
- mass spectrometry
- long non coding rna
- inflammatory response
- extracorporeal membrane oxygenation
- induced pluripotent stem cells
- peripheral blood
- climate change
- acute respiratory distress syndrome
- health information
- aortic dissection
- life cycle