Robert L. Hendricks, Ph.D.

Research Interests     Antigen presentation and co-stimulatory interactions at inflammatory sites. Herpes simplex virus (HSV) induces immunopathology in the cornea that leads to progressive scarring and blindness. CD4 T cells through Th1 cytokines mediate the inflammation in HSV-infected mouse corneas, providing an interesting and clinically important model for studying co-stimulatory requirements for activating CD4 T cells at sites of infection and inflammation. We are currently concentrating on the co-stimulatory signals required to activate CD4+ T cells in the infected cornea. Mechanisms of T cell control of HSV reactivation from latency in sensory neurons. During primary infection at mucosal surfaces, HSV infects sensory neurons, is transported to the cell bodies in the sensory ganglia, and there establishes a latent infection. Reactivation from latency results in recurrent herpetic disease. We recently demonstrated that CD8+ T cells that infiltrate the latently infected ganglion can prevent the virus from reactivating from a latent state. We are currently characterizing receptor specificity and function of the CD8+ T cells that are retained in the latently infected ganglia with the goal of developing vaccines or other means of augmenting this protective function.     Selected Publications     Freeman ML, Sheridan BS, Bonneau RH, Hendricks RL. Psychological stress compromises CD8(+) T cell control of latent herpes simplex virus type 1 infections. J Immunol 179:322-328. 2007. Sheridan BS, Khanna KM, Frank GM, Hendricks RL. Latent virus influences the generation and maintenance of CD8+ T cell memory. J Immunol 177:8356-8364. 2006. Decman V, Kinchington PR, Harvey SA, Hendricks RL. Gamma interferon can block herpes simplex virus type 1 reactivation from latency, even in the presence of late gene expression. J Virol 79:10339-10347. 2005. Khanna KM, Bonneau RH, Kinchington PR, Hendricks RL. Herpes simplex virus-specific memory CD8+ T cells are selectively activated and retained in latently infected sensory ganglia. Immunity 18:593-603. 2003. Liu T, Khanna KM, Chen X, Fink DJ, Hendricks RL. CD8(+) T cells can block herpes simplex virus type 1 (HSV-1) reactivation from latency in sensory neurons. J Exp Med 191:1459-1466. 2000.     Other Links     University of Pittsburgh

Office:  922 EEINS     Lab: 919 EEINS     Phone: 412.647.5754     Fax:412.647.5880     hendricksrr@upmc.edu     Academic Affiliations     Joseph F. Novak Professor and Vice-chair for Research, Department of Ophthalmology Professor, Departments of Immunology and Molecular Genetics and Biochemistry Member, University of Pittsburgh Cancer Institute Faculty member, McGowan Institute for Regenerative Medicine     Education     B.S. - University of Illinois Chicago M.S. - University of Illinois Chicago Ph.D. - University of Illinois Chicago     Grant Support     Title: Gene Expression in HSV-1 Latency After Corneal Infection Agency: NIH Funding Period: 2004-2008 Title: Role of cytotoxic lymphocytes in HSV-1 corneal lesions Agency: NIH Role: P.I. Funding Period: 1986-2008 Title: Cytokines and adhesion molecules in HSV keratitis Agency: NIH Role: P.I. Funding Period: 1993-2012 Title: Core Grant For Vision Research Agency: NIH Role: P.I. Funding Period: 1989-2009           Lab Personnel     Faculty Thomas L. Cherpes, M.D. Graduate Students Brian Sheridan Gregory Frank Jared Knickelbein Technician Dawn Maker James Busch Jessica Spehar           Click here for University of Pittsburgh Interdisciplinary Biomedical Graduate Program Website