Karin E. Peterson, Ph.D.Rocky Mountain LaboratoriesBldg 1, Room 1111903 South 4th Street Hamilton, MT 59840-2932Phone: email@example.com
Karin Peterson, 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 (RML) 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 2004, 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 RML as a tenure-track investigator to study the innate immune responses in the CNS and their role in viral pathogenesis.
CNS Virus infection of the central nervous system (CNS) often results in damage to neurons and the development of neurological disease. Multiple cell types in the CNS are activated during virus infection and may play important roles in regulating viral pathogenesis. The goal of our laboratory is to determine how the innate immune responses of intrinsic brain cells such as astrocytes, microglia and neurons influence viral pathogenesis in the CNS with the ultimate goal of identifying targets for therapeutic treatment of viral-mediated neurological diseases. To examine the role of innate immune responses in the CNS, we utilize an indirect model of retroviral pathogenesis in the CNS. In this model, neurons are not directly infected but disease is induced through the activation of glial cells, reminiscent of what is observed with HIV infection in the CNS. We also examine the innate response of neurons to direct viral infection using La Crosse Virus (LACV), a bunyavirus which is one of the leading causes of pediatric viral encephalitis in the United States. Additionally, we are examining the direct effects of individual components of the innate immune response in triggering activation and damage of cells in the CNS using targeted activation of pattern recognition receptors in primary cultures of neuronal and glial cells.
(View list in PubMed.)
Du. M, Butchi, N.B. Woods, T. and Peterson, K.E. 2011. Poly-thymidine oligonucleotides mediate activation of murine glial cells primarily through TLR7, not TLR8. PLoS One, in press.
Butchi NB, Woods T, Du M, Morgan TW and Peterson KE. 2011. TLR7 and TLR9 trigger distinct neuroinflammatory responses in the CNS. A.J. Pathol, in press.
Mukherjee P, Butchi NB and Peterson KE. 2011. Pattern Recognition Receptor activation of intrinsic brain cells and influence on viral neurovirulence. In Neuroinflammation: Pathogenesis, Mechanisms and Management. NOVA publishing, in press.
Du M, Butchi NB, Woods T, Morgan TW, Peterson KE. 2010. Neuropeptide Y has a protective role during murine retrovirus induced neurological disease. J. Virology 84:11076-88.
Butchi NB, Du M, Peterson KE. 2010. Interactions between TLR7 and TLR9 agonists and receptors regulate innate immune responses by astrocytes and microglia. Glia. 58:650-64.
Peterson, KE and M Du 2009. Innate Immunity in the Pathogenesis of Polytropic Retrovirus Infection in the Central Nervous System. Immunol. Research. 43: 49-59.
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. 14: 492-502
Butchi NB, Pourciau S, Du M, Morgan TW, Peterson KE. 2008. 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.
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Last Updated June 29, 2011