Guillain-Barré syndrome (GBS) is an autoimmune disease in which the peripheral nerves are affected. GBS has different subtypes, such as acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). Infections, e.g. Campylobacter jejuni, influenza, etc., can lead to GBS. Both environmental and genetic factors play a major role in the occurrence of GBS. Several studies have investigated the genetic basis of GBS. Human leukocyte antigens (HLA) genes, Cluster of Differentiation (CD) 1A, FAS, Fc gamma receptors (FcGR), Intercellular adhesion molecule-1 (ICAM1), different interleukins, Nucleotide oligomerization domain (NOD), Toll-like receptor 4 (TLR4), Tumor necrosis factor-α (TNF-α) are among the genes reported to be involved in susceptibility to the disease. Dysregulation and dysfunction of the mentioned gene products, even though their role in the pathogenesis of GBS is controversial, play a role in inflammatory pathways, regulation of immune cells and system, antigen presentation, axonal degeneration, apoptosis, and cross-reaction. This review aims to summarize associated genes with GBS to contribute to better understanding of GBS pathogenesis and discover the gene pathways that play role in GBS occurrence.

格林-巴利综合征 (GBS) 是一种自身免疫性疾病，其中周围神经受到影响。GBS有不同的亚型，例如急性炎性脱髓鞘性多发性神经病（AIDP）和急性运动轴索神经病（AMAN）。感染，例如空肠弯曲杆菌、流感等，可导致 GBS。环境和遗传因素在 GBS 的发生中起主要作用。一些研究调查了 GBS 的遗传基础。人类白细胞抗原 (HLA) 基因、分化簇 (CD) 1A、FAS、Fc γ 受体 (FcGR)、细胞间粘附分子-1 (ICAM1)、不同的白细胞介素、核苷酸寡聚化结构域 (NOD)、Toll 样受体 4 ( TLR4)、肿瘤坏死因子-α (TNF-α) 是据报道与疾病易感性有关的基因之一。上述基因产物的失调和功能障碍，尽管它们在 GBS 发病机制中的作用存在争议，但在炎症通路、免疫细胞和系统的调节、抗原呈递、轴突变性、细胞凋亡和交叉反应中发挥作用。