Immunology Graduate Group

Phillip Scott, Ph.D.

Professor of Immunology and

Associate Dean for Research, School of Veterinary Medicine

Address

310 B Hill Pavilion?School of Veterinary Medicine

380 S University Avenue, Philadelphia, PA 19104 ??Office tel.: 215 898-1602 and 215 898-9793;?Lab tel.: 215 898-0526?Fax: 215 746-2294

E-mail: pscott@vet.upenn.edu  

Assistant: Gayle Joseph viale@vet.upenn.edu

Education
Villanova University: BS (Biology), 1975

University of Pennsylvania: PhD (Parasitology), 1980

Research Interests

• T cells and cytokines in infectious disease
• Host-pathogen interactions
• Development of Th1 and Th2 cells
• Memory T cells

Key words: parasites, Leishmania, T cells, Th1 cells, Th2 cells, memory T cells.

 

Research Summary
  

Dr. Scott's current research is focused on understanding the development, regulation and maintenance of CD4+ Th1 and Th2 cells in order to design new vaccines and immunotherapies for infectious diseases. The laboratory primarily focuses on experimental murine infections with the protozoan parasite, Leishmania, which provides a well-characterized model of T helper cell differentiation. The use of IL-12 as an adjuvant to promote Th1 cell development, as well as the ability of combined drug and IL-12 therapy to promote a Th2 to Th1 switch, was first shown in this laboratory. Both findings have implications for the control and treatment of infectious diseases, autoimmunity and allergy. While much has been learned about the development of Th1 cells, our understanding of how to maintain Th1 responses-or cell-mediated immunity-is limited. This is highlighted by the fact that there is no vaccine for human leishmaniasis. Dr. Scott's laboratory is investigating the role of cytokines, antigen-dose, CD8+ T cells and antigen persistence in the development of immunologic memory. These studies indicate that a population of lymph node homing memory T cells, which have been called central memory T cells, are generated during Leishmania infection, and can be maintained in the absence of parasites. Future studies are directed at determining how to increase this population of memory T cells following vaccination. In related experiments, this laboratory has demonstrated that a Leishmania mutant, which lacks phosphoglycans and fails to induce disease, is maintained in vivo and protects mice against challenge with virulent organisms. Studies are in progress to characterize the immunity induced by these mutant parasites. Finally, studies are ongoing to understand how different species of Leishmania influence T helper cell subset development. While L. major induces a Th1 response and a healing infection in many strains of mice, the same strains of mice infected with parasites belonging to the L. mexicana complex fail to develop a Th1 response or heal. Thus, the laboratory is focused on defining the parasite virulence factors that modulate T helper cell development by different species of Leishmania.

Recent Publications   

Artis, D., L.M. Johnson, K. Joyce, C. Saris, A. Villarino, C. A. Hunter, and P. Scott. 2004. Cutting Edge: Early IL-4 production governs the requirement for IL-27/WSX-1 signaling in the development of protective Th1 cytokine responses following Leishmania major infection. J. Immunol. 172:4672-4675

Uzonna, J.E., K. Joyce, and P. Scott. 2004 Low dose Leishmania major promotes a transient T helper cell type 2 response that is downregulated by interferon-g producing CD8+ T cells. Journal of Experimental Medicine. 199:1559-1566.

Zaph, C., J. Uzonna, S. M. Beverley and P. Scott. 2004. Central memory T cells mediate long-term immunity to Leishmania major in the absence of persistent parasites. Nature Medicine 10:1104-1110.

Gray PM, Reiner SL, Smith DF, Kaye PM, Scott P.  2006 Antigen-experienced T cells limit the priming of naive T cells during infection with Leishmania major. J Immunol. 15;177(2):925-33.

Johnson, LM and Scott, P. 2007 STAT1 expression in dendritic cells, but not T cells, is required for immunity to Leishmania major.  J Immunol. 178 (11):7259-66.

 

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