Robert L. Hendricks, PhD

Contact

hendricksrr@upmc.edu

412-647-5754

Fax: 412-647-5880

922 Eye and Ear Institute

Education

PhD in Immunology, University of Illinois at Chicago

MS in Microbiology, University of Illinois at Chicago

Bs in Biology, University of Illinois at Chicago

Academic Affiliation(s)

Joseph F. Novak Professor and Vice-Chair for Research, Department of Ophthalmology

Director, Ophthalmology & Visual Sciences Research Center

Professor, Department of Microbiology and Molecular Genetics

Professor, Department of Immunology

Member, University of Pittsburgh Cancer Institute

Member, McGowan Institute for Regenerative Medicine

Member, Molecular Virology and Microbiology Graduate Program

Member, Immunology Graduate Program

Research

Dr. Hendricks' research focuses on three important aspects of the immune response to herpes simplex virus type 1 (HSV-1): HSV-1 induces immunopathology in the cornea of the eye that can lead to scarring and blindness. CD4 T cells through Th1 and Th17 cytokines mediate the inflammation in HSV-1 infected mouse corneas, providing an interesting and clinically important model for studying mechanisms of T cell-mediated inflammation and tissue destruction. The clarity of the corneal tissue permits direct observation of the developing inflammation, and the cornea facilitates manipulation of the T cell-antigen presenting cell interaction and local cytokine and chemokine functions, the focus of current studies.

When corneas become scarred by recurrent bouts of HSV-1 induced inflammation the only recourse is corneal transplantation. Unfortunately patients with recurrent HSV-1 corneal disease reject transplanted corneas at a very high rate. Our laboratory is employing a model of corneal transplantation in mice to study the mechanisms of accelerated corneal graft rejection in mice with previous HSV-1 corneal disease.

During primary infection at mucosal surfaces, HSV-1 invades sensory neurons, is transported to neuronal cell bodies in the sensory ganglia, and there establishes a latent (quiescent) infection. Reactivation from latency results in recurrent disease in innervated tissues including the cornea. Our laboratory first demonstrated that CD8 T cells provide active immunesurveillance of latently infected neurons, preventing reactivation from the latent state. We are currently characterizing T cell receptor specificity and function of CD8 T cells in latently infected sensory ganglia with the goal of developing vaccines or other means of augmenting their protective function.