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首页> 外文期刊>Vaccine >Prototype Alzheimer's disease epitope vaccine induced strong Th2-type anti-Abeta antibody response with Alum to Quil A adjuvant switch
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Prototype Alzheimer's disease epitope vaccine induced strong Th2-type anti-Abeta antibody response with Alum to Quil A adjuvant switch

机译：原型阿尔茨海默氏病抗原决定簇疫苗可引发明矾对Quil A佐剂转换的强Th2型抗Abeta抗体反应

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Beta-amyloid (Abeta) peptide has been proposed to be a causal factor in Alzheimer's disease (AD). Currently being investigated, active and passive Abeta-immunotherapy significantly reduce Abeta plaque deposition, neuritic dystrophy, and astrogliosis in the brains of APP transgenic (APP/Tg) mice. Immunization with Abeta42 formulated in the Th1-type adjuvant QS21 was beneficial for AD patients with significant titers of anti-Abeta antibodies, however, 6% of participants developed meningoencephalitis, likely due to anti-Abeta-specific autoimmune Th1 cells. Thus, successful Abeta vaccination requires the development of strong antibody responses without Th1-type cellular immunity. In this study, we compared the induction of humoral immune responses with Th1-type (Quil A) and Th2-type (Alum) adjuvants singly and in combination, using our novel epitope vaccine composed of self B cell epitope Abeta(1-15) and foreign T cell epitope PADRE (PADRE-Abeta(1-15)-MAP). Formulated in Quil A, this vaccine resulted in significantly higher anti-Abeta antibody responses in both BALB/c (H-2d) and C57BL/6 (H-2b) mice, compared with Alum. Anti-Abeta antibodies induced by Alum were predominantly IgG1 type accompanied by lower levels of IgG2a and IgG2b. Quil A induced robust and almost equal titers of anti-Abeta antibodies of IgG1 and IgG2a isotypes and slightly lower levels of IgG2b. Switching adjuvants from Alum to Quil A induced higher concentrations of antibodies than injections with Alum only, however slightly lower than Quil A only. Switching both adjuvants did not change the profile of antibody responses generated by the initial adjuvant injected. These results suggest that switching from Alum to Quil A would be beneficial for AD patients because anti-Abeta antibody production was enhanced without changing the initially generated and likely beneficial Th2-type humoral response.
机译：已经提出β-淀粉样蛋白（Abeta）肽是阿尔茨海默氏病（AD）的病因。当前正在研究中，主动和被动Abeta免疫疗法可显着减少APP转基因（APP / Tg）小鼠大脑中的Abeta斑块沉积，神经营养不良和星形胶质变。 Th1型佐剂QS21中配制的Abeta42免疫对具有显着效价的抗Abeta抗体的AD患者有益，但是，有6％的参与者发展了脑膜脑炎，这可能是由于抗Abeta特异性自身免疫性Th1细胞引起的。因此，成功的Abeta疫苗接种需要开发强大的抗体反应而无Th1型细胞免疫。在这项研究中，我们使用由自身B细胞抗原决定簇Abeta（1-15）组成的新型抗原决定簇疫苗，分别比较了Th1型（Quil A）和Th2型（Alum）佐剂对体液免疫反应的诱导作用。和外来T细胞抗原决定簇PADRE（PADRE-Abeta（1-15）-MAP）。与明矾相比，该疫苗以Quil A配制，在BALB / c（H-2d）和C57BL / 6（H-2b）小鼠中均产生明显更高的抗Abeta抗体应答。 Alum诱导的抗Abeta抗体主要为IgG1型，并伴有较低水平的IgG2a和IgG2b。 Quil A诱导产生强大且几乎相等的效价的IgG1和IgG2a同型抗Abeta抗体，以及稍低的IgG2b水平。与仅使用明矾注射相比，将佐剂从明矾转换为Quil A诱导的抗体浓度更高，但仅比Quil A低。切换两种佐剂都不会改变由最初注射的佐剂产生的抗体应答的概况。这些结果表明，从明矾转换为Quil A对AD患者将是有益的，因为在不改变最初产生且可能有益的Th2型体液反应的情况下，抗Abeta抗体的产生得以增强。

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