McMichael A J, Hall A J
Department of Epidemiology and Population Sciences, London School of Hygiene and Tropical Medicine, United Kingdom.
Epidemiology. 1997 Nov;8(6):642-5. doi: 10.1097/00001648-199710000-00005.
Multiple sclerosis is regarded as an autoimmune disease. The autoimmune process is thought to be triggered by early-life exposure to viral/bacterial antigens that share key peptide sequences with myelin protein (the target of autoimmune attack in multiple sclerosis). It has long been known that the incidence of multiple sclerosis is positively correlated with latitude, particularly in Caucasian populations. There is no agreed explanation for this latitude gradient, however. Ultraviolet radiation level is negatively correlated with latitude. Recent evidence suggests that ultraviolet-B is immunosuppressive, affecting particularly T-cell activity and delayed-type hypersensitivity. We hypothesize here that the latitude gradient of multiple sclerosis may reflect differential ultraviolet-induced suppression of autoimmune activity, particularly since the autoimmune profile of multiple sclerosis is characterized by disturbances of those T-cell-related activities that are specifically affected by ultraviolet-B. We propose some specific tests of this hypothesis.
多发性硬化被视为一种自身免疫性疾病。人们认为自身免疫过程是由早年接触与髓磷脂蛋白（多发性硬化中自身免疫攻击的靶点）共享关键肽序列的病毒/细菌抗原引发的。长期以来，人们已知多发性硬化的发病率与纬度呈正相关，尤其是在白种人群体中。然而，对于这种纬度梯度并没有一致认可的解释。紫外线辐射水平与纬度呈负相关。最近的证据表明，紫外线B具有免疫抑制作用，尤其会影响T细胞活性和迟发型超敏反应。我们在此假设，多发性硬化的纬度梯度可能反映了紫外线诱导的自身免疫活性抑制的差异，特别是因为多发性硬化的自身免疫特征表现为那些受紫外线B特异性影响的T细胞相关活动的紊乱。我们提出了对这一假设的一些具体测试。
