阿尔茨海默病患者外周淋巴细胞对Aβ1-40刺激反应性研究

The response of peripheral lymphocyte to amyloid fragment(Aβ1-40) in patients with Alzheimer's disease

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.