Hartung H P, Pollard J D, Harvey G K, Toyka K V
Department of Neurology, Julius-Maximilians-Universität, Würzburg, Germany.
Muscle Nerve. 1995 Feb;18(2):137-53. doi: 10.1002/mus.880180202.
The etiology of the Guillain-Barré syndrome (GBS) still remains elusive. Recent years have witnessed important advances in the delineation of the mechanisms that may operate to produce nerve damage. Evidence gathered from cell biology, immunology, and immunopathology studies in patients with GBS and animals with experimental autoimmune neuritis (EAN) indicate that GBS results from aberrant immune responses against components of peripheral nerve. Autoreactive T lymphocytes specific for the myelin antigens P0 and P2 and circulating antibodies to these antigens and various glycoproteins and glycolipids have been identified but their pathogenic role remains unclear. The multiplicity of these factors and the involvement of several antigen nonspecific proinflammatory mechanisms suggest that a complex interaction of immune pathways results in nerve damage. Data on disturbed humoral immunity with particular emphasis on glycolipid antibodies and on activation of autoreactive T lymphocytes and macrophages will be reviewed. Possible mechanisms underlying initiation of peripheral nerve-directed immune responses will be discussed with particular emphasis on the recently highlighted association with Campylobacter jejuni infection.
吉兰-巴雷综合征（GBS）的病因仍不明晰。近年来，在阐释可能导致神经损伤的机制方面取得了重要进展。从GBS患者及实验性自身免疫性神经炎（EAN）动物的细胞生物学、免疫学和免疫病理学研究中收集的证据表明，GBS是由针对周围神经成分的异常免疫反应所致。已鉴定出针对髓磷脂抗原P0和P2的自身反应性T淋巴细胞以及针对这些抗原和各种糖蛋白及糖脂的循环抗体，但其致病作用仍不明确。这些因素的多样性以及几种抗原非特异性促炎机制的参与表明，免疫途径的复杂相互作用导致了神经损伤。将综述关于体液免疫紊乱（特别强调糖脂抗体）以及自身反应性T淋巴细胞和巨噬细胞激活的数据。将讨论外周神经定向免疫反应起始的潜在机制，特别强调最近突出的与空肠弯曲菌感染的关联。
