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Ocular Immunology
Dr. John Oakes,
Professor, received his Ph.D. in Microbiology
from the University of Tennessee in 1975
and did his postdoctoral work at the Pennsylvania
State University College of Medicine, Milton
S. Hershey Medical Center. He was awarded
the Institute of
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of Allergy and
Infectious Disease Research Career Development
Award. He has served has a Member of of
The National Eye Institute Visual Sciences
Study Section. He is an ad hoc reviewer
for several journals related to immunology,
virology, and ophthalmology.
My laboratory is interested in ocular immunology
and the host's immune response to ocular
infections. The corneal surface is composed
of epithelial cells resting upon a layer
of connective tissue containing keratocytes.
It has recently become clear that damage
to the eye surface caused by ocular infections
induces epithelial cells and keratocytes
to synthesize and release cytokines and
chemokines. Cytokine and chemokine molecules
then enter the blood where they can recruit
immunologically active neutrophils, monocytes
and lymphocytes into the cornea. In the
process of mediating their immunological
functions at the eye surface, the cells
permanently damage the cornea leading to
corneal opacity and blindness.
The goal of our study is to investigate
the molecular biology of cytokine and chemokine
synthesis in the two major cell types of
the cornea. We are particularly
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interested in how the
genes for cytokines and chemokines are turn-on
in corneal cells and more importantly, how
they are turn-off once stress to the cornea
has been relieved. In some of these studies,
herpes simplex virus infection of humanbeen
relieved. In some of these studies, herpes
simplex virus infection of humancorneal
epithelial cells and keratocytes in vitro
is used as a model system to investigate
these questions.
An understanding of how genes for cytokines
and chemokines are regulated in the human
cornea can potentially lead to the development
of better therapeutic agents to control
inflammation at the eye surface and thereby
reduce the risk of vision loss.
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Recent
Publications
McInnis, K. A., A. Britain, R. N. Lausch, and J. E. Oakes. 2005. Synthesis of alpha-chemokines IP-10, I-TAC, and MIG are differentially regulated in human corneal keratocytes. Invest Ophthalmol Vis Sci (46):1668-74.
Ritchie, M. H., R. A. Fillmore, R. N. Lausch, and J. E. Oakes. 2004. A role for NF-kappaB binding motifs in the differential induction of chemokine gene expression in human corneal epithelial cells. Invest Ophthalmol Vis Sci (45):2299-305.
Bitko, V., N. E. Garmon, T. Cao, B. Estrada, J. E. Oakes, R. N. Lausch, and S. Barik. 2004. Activation of cytokines and NF-kappa B in corneal epithelial cells infected by respiratory syncytial virus: potential relevance in ocular inflammation and respiratory infection. BMC Microbiol (4):28.
Bevans-Nelson, S. E., R. N. Lausch, and J. E. Oakes. 2001. Tumor Necrosis Factor-alpha and not Interleukin-1alpha is the Dominant Inducer of Matrix Metalloproteinase-9 Synthesis in Human Corneal Cells. Exp Eye Res 73 (3):403-407
<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11520115&dopt=Abstract>.
Cubitt, C. L., R. N. Lausch, and J. E. Oakes. 2001. Synthesis of type II interleukin-1 receptors by human corneal epithelial cells but not by keratocytes. Invest Ophthalmol Vis Sci (42):701-4.
Tran, M. T., M. H. Ritchie, R. N. Lausch, and J. E. Oakes. 2000. Calcitonin gene-related peptide induces IL-8 synthesis in human corneal epithelial cells. J Immunol 164 (8):4307-4312. |
