【摘 要】
：
Three-month-old Alzheimer’s disease model transgenic mice were immunized with Aβ1-42, Plp-Adenovirus [Ad]-X-CMV-(Aβ3-10)10-CpG [AdCpG-(Aβ3-10)10] or AdCpG v
【机 构】
：
Department of Neurology, First Afifliated Hospital of China Medical University, Shenyang, Liaoning P
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Three-month-old Alzheimer’s disease model transgenic mice were immunized with Aβ1-42, Plp-Adenovirus [Ad]-X-CMV-(Aβ3-10)10-CpG [AdCpG-(Aβ3-10)10] or AdCpG virus lfuid via na-sal mucosal inhalation, respectively. ELISA analysis of serum showed Aβ42 antibody titers were signiifcantly increased in mice immunized with Aβ1-42 and AdCpG-(Aβ3-10)10. Concanavalin A and AdCpG-(Aβ3-10)10 stimulation signiifcantly increased the number of proliferating spleen cells cultured from AdCpG(Aβ3-10)10 and Aβ42 groups compared with the control group. In the AdCp-G(Aβ3-10)10 group, levels of interleukin (IL)-4 and IL-10 were increased, while those of IL-2 and interferon-γwere decreased. In the Aβ42 group, levels of IL-4, IL-10, IL-2 and interferon-γwere all increased. Experimental ifndings indicate that AdCpG-(Aβ3-10)10 vaccine can produce strong T helper 2 (hT2) humoral immune responses in addition to the production of Aβ42 antibody. hTe cellular immunologic response was weak and avoided Aβ1-42-mediated cytotoxicity.
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