Drew Weissman
Assistant Professor, Dept of Infectious Diseases

Microbiology, Virology and Parasitology Program

Address

522B Johnson Pavilion
3610 Hamilton Walk
Philadelphia, PA 19104-9999

Office tel.: 215 614-0291
Lab tel.: 215 662-3185
Fax: 215 349-5111
E-mail: dreww@mail.med.upenn.edu


Education

Brandeis University: BA/MA (Biochemistry), 1981.

Boston University: PhD (Immunology), 1987.

Boston University: MD, 1987.

Research Interests

• Immunopathogenesis.

Key words: HIV, Immunopathogenesis, RNAi, gp-340, dendritic cell, siRNA, antigen presentation, HIV vaccine.

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Description of Research

Dr. Weissman s laboratory focuses on the application of immunologically based basic science research principals to clinically relevant questions. The central theme of these projects is the study of dendritic cell (DC) biology and the application of these findings to vaccine research and HIV immunopathogenesis. As the most potent antigen-presenting cell and the only one capable of inducing naive immune responses, understanding DC function is critical in the development of new vaccine approaches to infectious and neoplastic diseases, in understanding the initiation and control of immune responses, and in exploring pathologic insults to the immune system. There are three main projects in his laboratory at the present time. The first uses mRNA and lentiviruses encoding antigen as a delivery system to load DC with antigen and promote broad immune responsiveness. The second project studies a newly discovered molecule found on DC, macrophages, and epithelial cells that binds HIV envelope with high affinity and is involved in HIV transmission, antigen acquisition, and immune activation. The third project studies Toll-like receptor recognition of RNA.

Recent Publications

Karikó, K., Ni, H, Capodici, J., Lamphier, M., and Weissman, D. mRNA is an endogenous ligand for Toll-like receptor 3. J. Biol. Chem. 279: 12542-12550, 2004.

Karikó, K., Bhuyan, P., Capodici, J., and Weissman, D. Small interfering RNAs mediate sequence-independent gene suppression and induce immune activation by signaling through Toll-like receptor 3. J. Immunol. 172:6545-9, 2004.

Bhuyan, P.K., Karikò, K., Capodici, J., Lubinski, J., Hook, L., Friedman, H., and Weissman, D. siRNA-mediated inhibition of HSV-1 gene expression and function during infection of human keratinocytes. J. Virol. 78:10276-81, 2004

Karikó, K., Weissman, D., and Welsh, F.A. Inhibition of Toll-like receptor and cytokine signaling — a unifying theme in ischemic tolerance. In Press Journal of Cerebral Blood Flow and Metabolism.

Kariko, K., Buckstein, M., Ni, H.. Weissman, D. Suppression of RNA recognition by Toll-like receptors: the impact of RNA ontogeny and nucleoside modification. In Press, Immunity.

Lab

Rotation Projects for 2006-2007

• gp340 binding of HIV as a cofactor in cell transfer and infection.
• TLR3, TLR7, and TLR8 recognition of RNA
• Delivery of antigen encoding modified RNA as a therapeutic agent

Lab personnel:

Prakash Bhuyan
Gerogetta Cannon
Kathy Fernando
Houping Ni
Robbert Rennert
Earl Stoddard