Yan W X, Archelos J J, Hartung H P, Pollard J D
Department of Neurology, Institute of Clinical Neurosciences, Royal Prince Alfred Hospital and University of Sydney, Australia.
Ann Neurol. 2001 Sep;50(3):286-92. doi: 10.1002/ana.1129.
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is widely regarded as an autoimmune disorder, although the autoantigen remains unknown. In this study, the sera of 21 CIDP patients were examined by immunofluorescence for antimyelin activity and by Western blotting for binding to myelin proteins. Six sera contained anti-P0 immunoglobulin G antibodies, and four of these caused conduction block and demyelination following intraneural injection in experimental animals. Absorption with P0 protein eliminated the demyelinating activity. These results show that P0 is an autoantigen in some patients with CIDP. Since P0 possesses powerful adhesion properties and is largely responsible for myelin compaction, the demonstration of demyelination by human anti-P0 antibodies provides new insight into this important and common immunopathological process.
慢性炎性脱髓鞘性多发性神经根神经病（CIDP）尽管自身抗原尚不明确，但被广泛认为是一种自身免疫性疾病。在本研究中，通过免疫荧光检测21例CIDP患者血清的抗髓鞘活性，并通过蛋白质印迹法检测其与髓鞘蛋白的结合情况。6份血清含有抗P0免疫球蛋白G抗体，其中4份在实验动物神经内注射后导致传导阻滞和脱髓鞘。用P0蛋白吸收可消除脱髓鞘活性。这些结果表明，P0是部分CIDP患者的自身抗原。由于P0具有强大的黏附特性且在很大程度上负责髓鞘压实，人抗P0抗体导致脱髓鞘的证明为这一重要且常见的免疫病理过程提供了新的见解。
