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Faculty
 
Russ_little.jpg Russell D. Salter , Ph.D.
Professor
E1052 BST (Office)
E1006 BST (Lab)
Pittsburgh, PA 15261
Phone: 412.648.9471
Email: rds@pitt.edu
Fax: 412.383.8096
Faculty Research Interests
 
Research Interests
My laboratory is interested in designing subunit vaccines that stimulate CD8+ T cell responses against pathogens and tumor antigens, and the development of immunization strategies in animal models for eventual use in humans. Other projects are focused on the effects of cholesterol-dependent cytolysins such as listeriolysin O and anthrolysin O on the antigen presenting function of dendritic cells. How these products of gram-positive bacteria stimulate both systemic and local inflammation is being investigated. The role of P2X7 purinergic receptor in inducing IL-1beta secretion by macrophages is also under investigation, with the goal of identifying novel targets for anti-inflammatory intervention.
 
Education
  • B.S. - Virginia Polytechnic Institute and State University (1980)
  • Ph.D. - Duke University (1985)
  • Postdoc - Stanford University (1986-1989)
 
Academic Affiliation
  • Professor, Department of Immunology, University of Pittsburgh School of Medicine
  • Member, University of Pittsburgh Cancer Institute
 
Selected Publications
Watkins, SC, and Salter, RD. Functional Connectivity between Immune Cells Mediated by Tunneling Nanotubules. Immunity 23:1-10, 2005.

Chu, J, Thomas LM, Watkins, SC, Franchi, L, Nunez, G, and Salter RD. Cholesterol-dependent cytolysins induce rapid release of mature IL-1? from murine macrophages in a NLRP3 inflammasome and cathepsin B-dependent manner. J. Leuk. Biol., 86: 1227-1238, 2009.

Salter RD and Watkins SC. Dendritic cell altered states: what role for calcium? Immunological Reviews, 231:278-288, 2009.

Sun, C, Chu, J, Singh, S, and Salter, RD. Identification and characterization of a novel variant of the human P2X7 receptor resulting in gain of function. Purninergic Signal, 6:31-45, 2010.

Thomas, LM, and Salter, RD. Activation of macrophages by P2X7-induced microvesicles from myeloid cells is mediated by phospholipids and is partially dependent on TLR4. J. Immunol. E-pub ahead of print, Aug 13, 2010.
 
Grants
  • Title: Dendritic Cell Biology and Therapy Program
    Agency: NIH
    Role: Project 1 Leader
    Funding Period: 2004-2009

  • Title: Interaction of microvesicles and bacterial toxins with immune cells
    Agency: NIH
    Role: P.I.
    Funding Period: 2007-2012

  • Title: Modeling Immunity for Biodefense
    Agency: NIH/NIAID
    Role: Co-investigator
    Funding Period: 2005-2010

  • Title: University of Pittsburgh Center for HIV Protein Interactions (PCHPI)
    Agency: NIH
    Role: Co-investigator
    Funding Period: 2007-2012

  • Title: In Vivo PIB Amyloid: Imaging Normals, MCI & Dementia
    Agency: NIH
    Role: Co-investigator
    Funding Period: 2008-2010
 
Lab Personnel
Research Specialist
Sarita Singh

Graduate Student Researchers
Michelle Heid

Postdoctoral Fellow
Chengqun Sun
Peter Keyel
 
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