Robert L. Hendricks, Ph.D.

Robert L. Hendricks, Ph.D.


Office: 922 EEINS

Lab: 919 EEINS

Ph: 412-647-5754

Fax: 412-647-5880


  • B.S. - University of Illinois Chicago
  • M.S. - University of Illinois Chicago
  • Ph.D. - University of Illinois Chicago

Academic Affiliation

  • 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

About 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.

Selected Publications

Frank, G. M., A. J. Lepisto, M. L. Freeman, B. S. Sheridan, T. L. Cherpes, and R. L. Hendricks. 2010. Early CD4(+) T cell help prevents partial CD8(+) T cell exhaustion and promotes maintenance of Herpes Simplex Virus 1 latency. J.Immunol. 184:277-286.

Sheridan, B. S., T. L. Cherpes, J. Urban, P. Kalinski, and R. L. Hendricks. 2009. Reevaluating the CD8 T-cell response to herpes simplex virus type 1: involvement of CD8 T cells reactive to subdominant epitopes. J.Virol. 83:2237-2245.

Knickelbein, J. E., K. M. Khanna, M. B. Yee, C. J. Baty, P. R. Kinchington, and R. L. Hendricks. 2008. Noncytotoxic lytic granule-mediated CD8+ T cell inhibition of HSV-1 reactivation from neuronal latency. Science 322:268-271.