Karin E. Peterson, Ph.D.
Chief, Neuroimmunology Unit
Investigator
Neuroimmunology Unit
Karin Peterson, Ph.D., received her Ph.D. degree in microbiology and immunology in 1998 from the University of Missouri Medical School, where she studied autoimmunity and the activation of self-reactive T cells.
She then went to Rocky Mountain Laboratories in 1998 as a postdoctoral fellow in the Laboratory of Persistent Viral Diseases and applied her skills in immunology toward understanding the mechanisms that control the immune response to retrovirus infection. During this time, she became interested in the immune responses to virus infections in the central nervous system (CNS).
In 2003, Dr. Peterson accepted a position as an assistant professor at Louisiana State University School of Veterinary Medicine, where she furthered her studies on viral pathogenesis in the CNS and also taught classes in immunology and virology.
In 2008, she returned to Rocky Mountain Laboratories as a tenure-track investigator to study the innate immune responses in the CNS and their role in viral pathogenesis.
Description of Research Program
The activation and cytokine/chemokine production by resident glial cells is a common response of various types of CNS insults, including virus infections as well as neurological diseases of unknown etiologies. The primary focus of the Neuroimmunology Unit is to examine the events that trigger the initiation of neuroinflammatory responses in the CNS and the impact of glial activation on neurodegeneration.
The laboratory uses both in vivo and in vitro models to examine the roles of pattern recognition receptors (PRRs) in the activation of glial cells, the production of proinflammatory cytokines and chemokines, and the impact of these responses on neuronal survival. The laboratory also addresses the questions using mouse models of CNS virus infections to examine whether specific components of the innate immune response influence viral pathogenesis in the CNS.
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| Chemokine expression (red stain) by brain capillary endothelia cells in the CNS following TLR7 stimulation. |
Research Group Members
Left to right: Niranjan Butchi, Karin Peterson, Min Du. Not pictured: Tyson Woods.
Selected Publications
(View list in PubMed.)
Lewis SD, Butchi NB, Khaleduzzaman M, Morgan TW, Du M, Pourciau S, Baker DG, Akira S, Peterson KE. Toll-like receptor 7 is not necessary for retroviral neuropathogenesis but does contribute to virus-induced neuroinflammation. J Neurovirol. 2008 Nov 17:1-11. Epub ahead of print.
Peterson KE, Du M. Innate immunity in the pathogenesis of polytropic retrovirus infection in the central nervous system. Immunol Res. 2008 Sep 26. Epub ahead of print.
Peterson KE, Pourciau S, Du M, Lacasse R, Pathmajeyan M, Poulsen D, Agbandje-McKenna M, Wehrly K, Chesebro B. Neurovirulence of polytropic murine retrovirus is influenced by two separate regions on opposite sides of the envelope protein receptor binding domain. J Virol. 2008 Sep;82(17):8906-10.
Butchi NB, Pourciau S, Du M, Morgan TW, Peterson KE. Analysis of the neuroinflammatory response to TLR7 stimulation in the brain: comparison of multiple TLR7 and/or TLR8 agonists. J Immunol. 2008 Jun 1;180(11):7604-12.
Khaleduzzaman M, Francis J, Corbin ME, McIlwain E, Boudreaux M, Du M, Morgan TW, Peterson KE. Infection of cardiomyocytes and induction of left ventricle dysfunction by neurovirulent polytropic murine retrovirus. J Virol. 2007 Nov;81(22):12307-15.
Corbin ME, Pourciau S, Morgan TW, Boudreaux M, Peterson KE. Ligand up-regulation does not correlate with a role for CCR1 in pathogenesis in a mouse model of non-lymphocyte-mediated neurological disease. J Neurovirol. 2006 Aug;12(4):241-50.
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