John Altman, Ph.D.

Microbiology & Immunology
- Ph.D., University of California, 1991
- B.S., Massachusetts Institute of Technology, 1984
Phone: (404) 727-5981
Address: Vaccine Center
Email: altman@microbio.emory.edu
Website: http://www.microbiology.emory.edu/altman/
Research Interests:
During my postdoctoral work with Dr. Mark Davis at Stanford University, I developed an important new technology to directly identify antigen-specific T cells by staining with tetrameric forms of soluble MHC/peptide complexes that have enhanced avidity for cells bearing specific T cell antigen receptors (TCR). Since coming to Emory, I have developed several research programs, all centered around use of this new technology to investigate many aspects of CD8+ T cell mediated immune responses to viral infections. These include basic studies in mouse models designed to answer questions about the factors contributing to the development of antigen-specific T cell repertoires, clinically relevant studies to assess immune function in HIV-infected individuals on potent anti-retroviral therapy, and applied studies to assess AIDS vaccine efficacy in a rhesus macaque model. Together with Rafi Ahmed, we are employing the LCMV model to investigate the basis of T cell memory and the development of the LCMV-specific T cell repertoires.
The tetramers were originally developed to study CD8+ responses to HIV, and the initial reagents were based on two HIV-peptide complexes with HLA-A*0201. The most surprising finding of those studies was that the frequency of CD8+ T cells for a specific epitope was as high as 2% of all CD8+ T cells. We plan to follow up these studies to examine the effects of highly active antiretroviral therapy (HAART) on the frequency and function of HIV-specific CD8+ T cells. The questions that we will address concern the contribution of chronic antigen stimulation to maintaining the specific cells at high frequency and the effect it has on function. In many patients with high viral burdens, we have found that the HIV-specific CD8+ T cells die upon in vitro stimulation with peptide and IL2. We plan to investigate this further to determine if this antigen induced cell death is relevant in vivo and if it represents an important mechanism used by the virus to escape the immune response.