Curcumin reduces expression of Bcl-2, leading to apoptosis in daunorubicin-insensitive CD34+ acute myeloid leukemia cell lines and primary sorted CD34+ acute myeloid leukemia cells |
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Authors: | Jia Rao Duo-Rong Xu Fei-Meng Zheng Zi-Jie Long Sheng-Shan Huang Xing Wu Wei-Hua Zhou Ren-Wei Huang Quentin Liu |
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Affiliation: | 1. Department of Molecular Immunology, Institute for Molecular Medicine, Huntington Beach, CA, 92647, USA 2. University of California, Irvine, Institute for Memory Impairments and Neurological Disorders, Irvine, CA, 92697, USA 3. Department of Microbiology, Mount Sinai School of Medicine, New York, NY, 10029, USA 4. Department of Microbiology and Immunology, University of Rochester, Rochester, NY, 14642, USA 5. Global Health and Emerging Pathogens Institute, Mount Sinai School of Medicine, New York, NY, 10029, USA 6. Department of Medicine, Division of Infection Diseases, Mount Sinai School of Medicine, New York, NY, 10029, USA
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Abstract: | Background Numerous pre-clinical studies and clinical trials demonstrated that induction of antibodies to the β-amyloid peptide of 42 residues (Aβ42) elicits therapeutic effects in Alzheimer's disease (AD). However, an active vaccination strategy based on full length Aβ42 is currently hampered by elicitation of T cell pathological autoreactivity. We attempt to improve vaccine efficacy by creating a novel chimeric flu vaccine expressing the small immunodominant B cell epitope of Aβ42. We hypothesized that in elderly people with pre-existing memory Th cells specific to influenza this dual vaccine will simultaneously boost anti-influenza immunity and induce production of therapeutically active anti-Aβ antibodies. Methods Plasmid-based reverse genetics system was used for the rescue of recombinant influenza virus containing immunodominant B cell epitopes of Aβ42 (Aβ1-7/10). Results Two chimeric flu viruses expressing either 7 or 10 aa of Aβ42 (flu-Aβ1-7 or flu-Aβ1-10) were generated and tested in mice as conventional inactivated vaccines. We demonstrated that this dual vaccine induced therapeutically potent anti-Aβ antibodies and anti-influenza antibodies in mice. Conclusion We suggest that this strategy might be beneficial for treatment of AD patients as well as for prevention of development of AD pathology in pre-symptomatic individuals while concurrently boosting immunity against influenza. |
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