Immunology Graduate Group
Carl H. June, M.D.
Professor, Department of Pathology and Laboratory Medicine
Investigator, Abramson Family Cancer Research Institute
Address: Biomedical Research Building II/III, Room 554
Office Phone: (215) 573-5745
Fax: (215) 573-8504
Email: cjune@mail.med.upenn.edu
Education:
B.S., Biology, US Naval Academy
M.D., Baylor College of Medicine
Research Interests
1. human T cell adoptive immunotherapy
2. T cell biology and mechanisms of costimulation
3. HIV pathogenesis mechanisms
*There are two themes in the laboratory. One is to develop and test novel forms of immunotherapy for cancer and chronic infections. The other project involves determining mechanisms of lymphocyte activation.*
Research Summary
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Creation of artificial antigen presenting cells for immunotherapy. Beads coated with anti-CD3 and anti-CD28 monoclonal antibodies cause efficient invitro activation and propagation of T cells that can be used for adoptive transfer |
Over the last five years my laboratory has been studying the potential use of adoptive immunotherapy for HIV infection. We have developed a large-scale tissue culture technique that permits the efficient propagation of polyclonal HIV CD4 and CD8 T cells from patients with HIV infection. Several clinical trials involving adoptive immunotherapy of autologous and allogeneic T cells are in process. We plan to combine these with autologous dendritic cells. Our long-term goal is to be able to adoptively transfer autologous T cells and dendritic cells to unprimed individuals in order to induce an MHC class II restricted response. This would involve efficient ex vivo priming of na´ve CD4 T cells. Other trials involve infusions of gene modified T cells. Another project in the laboratory is T cell signal transduction. For the past ten years these studies have been focused on CD28 and CTLA-4. More recently we have also been studying mechanisms that regulate chemokine receptor expression and signal transduction in T cells. In addition, we are studying the role of telomerase expression in telomere maintenance and replicative senescence in T cells.
Recent Publications
Riley, J. L., B. L. Levine, N. Craighead, T. Francomano, Kim D, R. G. Carroll, and June C.H. 1998. Naive and memory CD4 T cells differ in their susceptibility to HIV-1 infection following CD28 costimulation: Implications for transmission and pathogenesis. J Virol. 72:8273-8280.
Kaushal, S., A. L. Landay, M. Lederman, Connick E, Spritzler J, Kuritzkes DR, Kessler H, B. L. Levine, D. St.Louis, and June C.H. 1999. Increases in T-cell telomere length in HIV infection after antiretroviral combination therapy for HIV-1 infection implicate distinct population dynamics in CD4+ and CD8+ T-cells. Clinical Immunology 92:14-24.
Blair PJ, Riley JL, Harlan DM, White L, Francomano T, Perfetto SJ, Kirk AD, and June CH. 2000. CD40 Ligand (CD154) Triggers a Short-Term CD4(+) T Cell Activation Response That Results in Secretion of Immunomodulatory Cytokines and Apoptosis. J Exp.Med. 191:651-660.
Riley, J.L., Schlienger, K., Blair PB, Carreno, B.M., Craighead, N., Kim, D., Carroll, R.G., and June C.H. 2000. Modulation of susceptibility to HIV-1 infection by