Luis Sigal, DVM, PhD
333 Cottman Avenue
Philadelphia, PA 19107
Philadelphia, PA 19107
Most Recent Peer-reviewed Publications
- The natural killer cell dysfunction of aged mice is due to the bone marrow stroma and is not restored by IL-15/IL-15Rα treatment
- CD4+ T cell help is dispensable for protective CD8+ T cell memory against mousepox virus following vaccinia virus immunization
- Protective CD8+ T cell memory without help
- Impact of distinct poxvirus infections on the specificities and functionalities of CD4+ T cell responses
- MyD88-dependent immunity to a natural model of vaccinia virus infection does not involve toll-like receptor 2
Member, Basic Science Division
Fox Chase Cancer Center
Research and Clinical Interests
My laboratory has two programs, both highly relevant to vaccines:
- Antigen presentation in viral infections. In this program we are studying the mechanisms whereby antigen presenting cells initiate CD8+ T cell responses in viral infections. This is an important area of research for vaccine development in as much asmemory CD8+ T cells induced by vaccination can protect against acute viral diseases (PNAS 104:10992,2007). This project is funded by R01A1048849.
- Mechanisms of natural and acquired resistance to ectromelia virus. In this program we are trying to understand the mechanisms of innate and acquiredimmunity that contribute to resistance to viral disease. Our model is ectromelia virus, the murine equivalent of human smallpox. Particularly relevant to vaccines, in a project funded by R01AI065544, we have recently found that a non-structural secreted factor encoded by poxviruses (the type I interferon binding protein) is essential for virulence and an effective target for antibody-mediated protection (J. Exp Med., revised manuscript submitted). Within this program we are also using ectromelia virus to pinpoint the specific immune functions affected by age that correlate with the loss of natural and acquired resistance to mousepox. The long term goal of this project is to find new methods to manipulate the immune response to restore resistance and improve vaccine efficacy in aged mice as a first approach to improve vaccine efficacy in elderly people. This project is funded by R21A1077021.