Rostami A M
Department of Neurology, University of Pennsylvania Medical Center, Philadelphia 19104, USA.
J Infect Dis. 1997 Dec;176 Suppl 2:S160-3. doi: 10.1086/513794.
Lewis rats immunized with P2 protein, a 14.5-kDa protein of the peripheral nerve myelin, develop experimental allergic neuritis, a paralytic disorder with clinical, histologic, and electrophysiologic features similar to those of human Guillain-Barré syndrome (GBS). T cells reactive to P2 protein or a peptide corresponding to 53-78 residues of the protein can transfer the disease to naive animals. The mechanisms by which these T cells induce demyelination are not well understood; however, they may induce inflammation and demyelination in the nerves by production of Th1 cytokines. Th2 cytokines may lead to suppression of the inflammation and eventual recovery. There is no conclusive evidence that P2 protein plays a role in the pathogenesis of GBS, with or without association with Campylobacter jejuni; however, studies of the immunopathogenesis of P2 protein-induced experimental allergic neuritis are important for understanding the pathogenesis of inflammatory demyelination in the peripheral nerves, the hallmark of GBS.
用外周神经髓鞘的14.5 kDa蛋白P2免疫的Lewis大鼠会发生实验性变应性神经炎，这是一种具有与人类吉兰-巴雷综合征（GBS）相似的临床、组织学和电生理特征的麻痹性疾病。对P2蛋白或对应于该蛋白53 - 78个残基的肽有反应的T细胞可将疾病传染给未接触过该抗原的动物。这些T细胞诱导脱髓鞘的机制尚不完全清楚；然而，它们可能通过产生Th1细胞因子在神经中诱导炎症和脱髓鞘。Th2细胞因子可能导致炎症的抑制并最终恢复。没有确凿证据表明P2蛋白在GBS的发病机制中起作用，无论是否与空肠弯曲菌有关联；然而，对P2蛋白诱导的实验性变应性神经炎的免疫发病机制的研究对于理解外周神经炎症性脱髓鞘（GBS的标志）的发病机制很重要。
