躁症患者抗熱休克蛋白 -60 、 -70 及 -90 自體 抗體之分析

躁症患者抗熱休克蛋白 -60 、 -70 及 -90 自體 抗體之分析

 有許多文獻證據顯示中樞神經系統與免疫系統間有密切的交互作用，比較特 別的是有關精神壓力與精神疾病患者有免疫異常情形的描述。目前學者提出 精神裂症患者有單核細胞與 T 細胞活化的假說，也有學者提出自體免疫機制 可能是精神分裂症的發病因素之一。躁鬱症是一種可能會出現躁狀精神狀態 的情感性疾病，目前有關躁症的免疫研究較少且結果仍有爭議，因此本實驗 的目的主要是研究單核細胞與 T 細胞所分泌的細胞激素的表現情形，以及躁 症患者可能存在的自體免疫抗體。 T 細胞與單核細胞的數目在躁症患者與正 常控制組相比沒有改變，躁症患者血清中 sIL-2R 的濃度有意義的高於正常控 制組，由 PHA 所刺激產生之 IFN-g 的濃度在躁症患者急性期與緩解期皆明顯 有意義的低於控制組，由 LPS 所刺激的單核細胞激素中只有 LIF 有意義的高 於正常組。總而言之，這些結果顯示雙極性情感疾病的免疫病生理機制可能 受症狀嚴重程度的影響，且調節機轉與正常人不同。另外，本實驗還利用西 方點墨法來檢測躁症患者血清樣本中與 U-373 MG 神經母細胞瘤細胞株蛋白 萃取物結合的抗體。有 19.6﹪ 的躁症患者與 10.6﹪ 的正常控制組表現對抗 60 kDa 蛋白的抗體，還有 7.2% 的患者與 15.2% 的正常人會表現對抗 100-120 kD a 蛋白的抗體，而上述這些抗體為何則需再進一步確認。

Analysis of Anti-Heat Shock Protein 60, -70 and -9 0 Autoantibodies in Patients with Manic Episode

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A close interaction between the central nervous system and the immune system have evidence d in many documents, in which we have paid attention to the study of immunological abnorma lities both in psychological stress and patients with psychotic disorder. More specifically, an a utoimmune mechanism was suggested as one of the possible factors in the pathogenesis of sch izophrenia. The aim of this study was to investigate the presence of antibodies that react with heat shock proteins (Hsps) in sera from patient with mania. The sera were tested for antibodies binding to cell extracts of U-373MG glioblastoma cell line using western blot analysis. Hsps a re intracellular proteins in most cells which are thought to serve protective functions against in fection and cellular stress. In some instances, Hsps may be aberrantly expressed on target tissu es interaction with the immune system might potentially result in autoimmune disease, as sugg ested in juvenile diabetes mellitus or rheumatoid arthritis.

In the part of autoantibodies against Hsp90, we observed that un-medicated acute patients wer

e significantly higher compared with remission patients. Sera anti-Hsp90 autoantibodies in me

dicated acute patients were significantly lower compared with un-medication acute patients. S

era anti-Hsp 70 and 90 autoantibodies in medicated acute patients were significantly lower co

mpared with normal controls. In addition, there was no significant difference on autoantibodie

s against Hsp60 between patients and normal controls . We suggested that a presence of abnor

mal immune reactivity involving Hsp90 in patients with manic acute episode, and it may impli

cate in pathogenesis in acute episode with this disease.