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机构地区:[1]中山医科大学附属第一医院神经科,广州510080 [2]广州市老人院
出 处:《中国神经精神疾病杂志》2001年第3期196-198,共3页Chinese Journal of Nervous and Mental Diseases
基 金:国家自然科学基金资助(编号:39370264)
摘 要:目的 探讨阿尔茨海默病(AD)外周淋巴细胞免疫功能的变化。方法 淀粉样蛋白肽(Aβ1-40)等刺激AD患者外周淋巴细胞,测定其增殖功能和凋亡细胞比例;异硫氰酸荧光素(FITC)标记单抗直接标记,流式细胞仪测定T细胞亚群。结果 轻、中~重AD组淋巴细胞对Aβ1-40刺激的增殖能力都显著低于对照;白介素-2(IL-2)分泌、白介素-2受体(IL-2R,CD25)表达和T细胞亚群及细胞凋亡在各组间无差异。结论 AD病人淋巴细胞对Aβ1-40刺激增殖反应低下,提示AD患者对Aβ1-40清除能力减弱可能与AD发病有关。Objective To study the role of immune dysfunction in the pathogenesis of Alzheimer's disease(AD). Methods Our patients were divided into two groups(mild and moderately severe AD) according to severity of disease, and their lymphocytes were compared to those of elderly controls. Lymphocytes were stimulated with amyloid fragment(Aβ1-40), and we analyzed the proliferative ability of interleukin 2(IL-2) secretion, cell membrane interleukin 2 receptor(IL-2R, CD25) expression, and cell apoptosis. Monoclonal antibodies labeled by FTTC were used for lymphocyte subset analysis. Results The stimulation index(SI) of both mild and moderately severe AD was significantly lower than that of controls( P < 0.05) . Measurement of IL-2 production levels, IL-2R expression, T lymphocyte subpopulations, and the amount of cell apoptosis revealed no significant differences between different groups. Conclusions These results suggest that lymphocytes with specificity for metabolic products of APP occur in health individuals. The ability of eliminate Aβ1-40 could be impaired in AD.
关 键 词:阿尔茨海默病 淀粉样蛋白肽 淋巴细胞 免疫功能 细胞因子
分 类 号:R749.161[医药卫生—神经病学与精神病学]
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