Research Interests
Dr. Chackerian's laboratory is interested in vaccine development; particularly the use of virus particles as platforms for antigen display. It has long been recognized that highly dense repetitive antigens such as virus particles induce strong immune responses. However, more recent studies from Dr. Chackerian's laboratory has demonstrated that normally poorly immunogenic antigens can be made highly immunogenic by linking them and presenting them to the immune system on the surface of virus particles. Dr. Chackerian has shown that this ability to enhance immunogenicity does not only apply to epitopes derived from traditional targets, such as pathogens, but also to self-antigens which are normally subject to the mechanisms of B cell tolerance. Thus, a major focus of his work is to develop new vaccines against self-antigens that are involved in disease processes. Dr. Chackerian has funded studies to develop vaccines against the HIV-1 receptor CCR5 (for HIV infection), and Amyloid-beta (for Alzheimer's Disease). He is collaborating closely with Dr. David Peabody in the department to develop a new phage display system for the rapid identification of new vaccines. He is also working with Dr. Hugh Smyth in the School of Pharmacy on the development of strategies for aerosol delivery of VLP-based immunogens.
Selected Publications
Peabody, D. S., Manifold-Wheeler, B., Medford, A., Jordan, S. K. Caldeira, J., and B. Chackerian (2008). Immunogenic Display of Diverse Peptides on Virus-Like Particles of RNA Phage MS2. Journal of Molecular Biology, 380, 252-263.
Chackerian, B. Durfee, M. R., and J. T. Schiller (2008). Virus-like Display of a Neo-self Antigen Reverses B cell Anergy in a B cell Receptor Transgenic Mouse Model. Journal of Immunology, 180 (9), 5816-5825.
B. Chackerian (2007). Virus-like Particles: Flexible Platforms for Vaccine Development. Expert Reviews of Vaccines 6 (3), 381-390.
Chackerian, B., Rangel, M., Hunter, Z., and D. S. Peabody (2006). Virus and virus-like particle based immunogens for Alzheimer's disease induce antibody responses against Amyloid-Beta without concomitant T cell responses. Vaccine 24 (37-39), 6321-6331.
Chackerian, B., Briglio, L., Albert, P. S., Lowy, D. R., and J. T. Schiller (2004). Induction of autoantibodies to CCR5 in macaques and subsequent effects upon challenge with an R5-tropic Simian/Human Immunodeficiency Virus. Journal of Virology 78 (8), 4037-4047.
Li, Q., Cao, C., Chackerian, B., Schiller, J. T., Gordon, M., Ugen, K. E., and D. Morgan (2004). Overcoming Antigen Masking of Anti-Abeta Antibodies Reveals Breaking of B cell Tolerance in Abeta Immunized Amyloid Precursor Protein Transgenic Mice. BMC Neuroscience 5: 21 (8 June 2004).
Chackerian, B., Lenz, P., Lowy, D. R., and J. T. Schiller (2002). Determinants of autoantibody induction by conjugated papillomavirus virus-like particles. Journal of Immunology 169 (11), 6120-6126.
Chackerian, B., Lowy, D. R., and J. T. Schiller (2001). Conjugation of a self-antigen to papillomavirus-like particles allows for efficient induction of protective autoantibodies. Journal of Clinical Investigation 108 (3), 415-423.
Chackerian, B., Lowy, D. R., and J. T. Schiller (1999). Induction of auto-antibodies to mouse CCR5 with recombinant papillomavirus particles. Proceedings of the National Academy of Sciences USA 96 (5), 2373-2378.