STUDIES OF THE IMMUNE SYSTEM IN SCHIZOPHRENIA

我们建议研究精神分裂症患者的免疫系统，以便 找出是否存在任何与相应的 控制病人。已经确定某些精神分裂症患者 严重迟发性运动障碍(TD)患者抗体效价升高 对抗人乙酰胆碱受体。这些针对受体的抗体 被发现是因为有可能纯化和标记受体； 但滴度虽然很高，但很低，这可能不一定 在TD或精神分裂症中牵涉到乙酰胆碱受体。这些 3例均无重症肌无力的临床体征。抗精神病药 药物可通过以下方式诱导一系列自身抗体 刺激免疫系统的细胞或通过作用于细胞膜 以这种方式使蛋白质成分具有抗原性。这样的抗体 将很难检测到，因为我们不知道它们所针对的抗原 都是导演的。这种可能性将通过测量来进一步探索 抗体亚类、T细胞亚群、抗脑抗体和抗核抗体 抗体。由于抗精神病药物被认为是导致TD的原因，我们将比较药物 治疗患有和不患有TD的患者。长期服用这种药物 给大鼠服用长达6个月的药物会导致口腔面部综合征 它与人类的TD有相似之处。我们要检查的是 这些动物体内有抗神经元抗体或淋巴细胞的证据 大脑可能负责导致神经变化 运动障碍。

We propose to investigate the immune system in schizophrenics in order to find out if any abnormalities are present in comparison to the appropriate control patients. It has already been determined that some schizophrenic patients with severe tardive dyskinesia (TD) have elevated antibody titers against human acetylcholine receptor. These antibodies against receptor were discovered because it is possible to purify and label the receptor; but the titers, although significant, were low and this may not necessarily implicate acetylcholine receptors in TD or in schizophrenia. These patients had no clinical signs of Myasthenia Gravis. Neuroleptic medication may induce a whole spectrum of autoantibodies either by stimulating cells of the immune system or by acting upon cell membranes in such a way that protein components are rendered antigenic. Such antibodies would be difficult to detect as we do not know the antigens to which they are directed. This possibility will be further explored by measuring antibody subclasses, T-cell subsets, anti-brain antibodies and anti-nuclear antibodies. As neuroleptics are thought to cause TD we will compare drug treated patients with and without TD. The chronic administration of such drugs to rats for as long as 6 months results in an orofacial syndrome which bears resemblance to TD in humans. We will examine the brains of such animals for evidence of anti-neuronal antibodies or lymphocytes in the brain which could be responsible for the neurological changes which cause the dyskinesia.