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首页> 外文会议>Medical Research Colloquium >Immunologic and Tolerogenic Aspects of Amyloid Beta-Peptide: Implications for the Pathogenesis and Treatment of Alzheimer's Disease
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Immunologic and Tolerogenic Aspects of Amyloid Beta-Peptide: Implications for the Pathogenesis and Treatment of Alzheimer's Disease

机译：淀粉样蛋白β-肽的免疫和耐受性方面：对阿尔茨海默病的发病机制和治疗的影响

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Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School. 77 Ave. Louis Pasteur, Boston, MA 02115 Alzheimer's disease (AD) is marked by the progressive accumulation of amyloid beta-peptide (A beta), which appears to trigger neurotoxic and inflammatory cascades. We investigated microglia as A beta antigen-presenting cells (APCs) and their interaction with Abeta-reactive T-cells, as a potential cascade in AD pathology. We found that IFN-gamma-treated microglia were potent A beta APCs measured by T-cell reactivity to A beta 1-40 and A beta 1-42, the major accumulating peptides. In B6SJL mice transgenic for human APP under the prion promoter, chronic A beta accumulation in the circulation was associated with immune hyporesponsiveness, apparently due to the lack of T-cell help for antibody production. In preliminary studies in humans, we have identified A beta-reactive T-cells in peripheral blood lymphocytes with a stronger response seen to A beta 1-42 than to Abeta 1-40. Taken together, our results suggest that Abeta-reactive T-cells exist in humans and, depending on genetic background, may expand in response to A beta deposition in the brain and/or neu-rodegenerative cascades during aging. Further investigation of these endogenous immune responses to A beta in humans may determine whether they contribute to, or protect against, AD and also whether they are involved in immunological reactions to A beta vaccines used to treat AD.
机译：哈佛医学院的神经系统疾病，Brigham和妇女医院中心。 77 Ave.Louis Pasteur，波士顿，MA 02115 Alzheimer的疾病（AD）标志着淀粉样蛋白β-肽（β）的逐渐积累，这似乎引发神经毒性和炎症级联。我们研究了微胶质细胞作为β抗原呈递细胞（APC），以及与ABETA反应性T细胞相互作用，作为AD病理学中的潜在级联。我们发现IFN-Gamma处理的小胶质细胞有效的βAPC，通过T细胞反应性与β1-40和β1-42，主要积累肽测量。在B6SJL转基因小鼠朊病毒启动子控制下的人APP，在循环慢性的Aβ积累与免疫低反应相关联的，显然是由于缺乏对抗体产生的T细胞的帮助。在人类的初步研究中，我们已经在外周血淋巴细胞中鉴定了β-反应性T细胞，其对β1-42的反应更强，而不是Abeta 1-40。我们的结果表明，在人类中存在ABETA-反应性T细胞，并且根据遗传背景，可以在老化期间响应脑和/或新棒状级联级联的β沉积而扩张。进一步调查对人类的ββ的这些内源性免疫应答可以确定它们是否有助于或保护，或保护它们是否参与用于治疗广告的β疫苗的免疫反应。

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