Owen S J, Watson C M, Davison A N
Department of Neurochemistry, Institute of Neurology, London, England, U.K.
Clin Exp Immunol. 1990 Oct;82(1):86-92. doi: 10.1111/j.1365-2249.1990.tb05408.x.
In order to study the possible autoimmune basis of multiple sclerosis (MS) a quantitative method has been used to investigate breakdown of human myelin in vitro. We found that serum from MS patients and controls was generally devoid of any myelin degradative activity. However, isolated peripheral blood mononuclear cells from 43% of MS patients showed significant myelin degradative activity as did those from 61.5% of patients with rheumatoid arthritis (RA). Myelin degradation by cells was found in only 13% of patients with other neurological diseases and in no healthy controls. It is proposed that this non-specific peripheral cellular immune degradative activity originates from cells activated within the central nervous system of MS patients or the joints of individuals with RA. As a result, activity in the blood only indirectly reflects the ongoing inflammatory response at the primary site, accounting for the lack of correlation between changes in the blood and the clinical status of the MS patient. We further propose that the lack of in vitro myelin degradative activity in cells recovered from the cerebrospinal fluid is due to autoaggressive cells being sequestered to the brain.
为了研究多发性硬化症(MS)可能的自身免疫基础,采用了一种定量方法来体外研究人髓磷脂的降解情况。我们发现,MS患者和对照组的血清通常没有任何髓磷脂降解活性。然而,43%的MS患者分离出的外周血单个核细胞显示出显著的髓磷脂降解活性,类风湿性关节炎(RA)患者中有61.5%的外周血单个核细胞也显示出这种活性。仅13%的其他神经系统疾病患者的细胞出现髓磷脂降解,而健康对照组中未发现此现象。有人提出,这种非特异性外周细胞免疫降解活性源自MS患者中枢神经系统或RA患者关节内激活的细胞。因此,血液中的活性仅间接反映了原发部位正在进行的炎症反应,这解释了血液变化与MS患者临床状态之间缺乏相关性的原因。我们进一步提出,从脑脊液中回收的细胞缺乏体外髓磷脂降解活性是由于自身攻击性细胞被隔离在大脑中。