Julie K. Olson, PhD
Associate Professor, School of Dentistry
Associate Professor, School of Dentistry
Fellowship, Northwestern University, The Feinberg School of Medicine, Chicago (Microbiology-Immunology)
PhD, University of Iowa College of Medicine
BS, University of Wisconsin-LaCrosse
The immune response that occurs in the central nervous system (CNS) with two areas of study within this interest: (a) examining the role of the CNS resident immune cells, microglia, during the immune response following virus infection, during neurological diseases, or during neuropathic pain in the CNS (b) neuroimmunology and the role of virus infection on the development and progression of autoimmune disease in the CNS.
My research interest is in the immune response that occurs in the central nervous system (CNS) with two areas of study within this interest. The first area of study examines the role of the CNS resident immune cells, microglia, during the immune response following virus infection, during neurological diseases, or during neuropathic pain in the CNS. My research focuses on the microglia cells which are macrophage type cells which reside in the CNS. The blood brain barrier restricts the infiltration of peripheral immune cells into the CNS until an immune response has been initiated in the CNS by resident cells. Therefore, microglia are the first line of defense against injury, infection, or disease in the CNS. My research examines how microglia respond to infection, disease, or injury; how the response by microglia contributes to the overall immune response; and whether the response is helpful or harmful to the CNS. A focus of this project is to develop agents that can alter the immune response by microglia to be used as a therapeutic strategy for treatment of neurological diseases. My second area of study in neuroimmunology is the role of virus infection on the development and progression of autoimmune disease in the CNS. Specifically, we study a virus-induced model of multiple sclerosis (MS) in mice. MS is an autoimmune demyelinating disease affecting humans, predominantly females. Strong epidemiological evidence suggests that virus infections play a role in disease development as well as disease progression. My studies utilize a mouse model of virus-induced MS, Theiler’s murine encephalomyelitis virus (TMEV). TMEV infection of mice results in the development of an autoimmune mediated demyelinating disease beginning with clinical symptoms around 35 days post infection with a chronic progression in severity, eventually leading to ascending paralysis and death. My research focuses on the role of the innate immune response in the development and progression of the autoimmune response and disease. We have demonstrated that the innate immune response initiated following virus infection plays a critical role in development and progression of the autoimmune demyelinating disease, and we have developed possible therapies based on the innate immune response which when administered to mice diminished the development and progression of the autoimmune disease.
- J.K. Olson. 2013. Innate immune response affects the development and progression of Theiler’s virus- induced demyelinating disease. J. Neurovirol. In Press.
- Bowen, J.L. and J.K. Olson. 2013. IFN-gamma influences type I interferon response and susceptibility to Theiler’s virus-induced demyelinating disease. Virol Immunol. 26(4):223-38. PMID:23829778
- Y-P Liu, L. Zeng, A. Tian, A. Bomkamp, D. Rivera, D. Gutman, G.N. Barber, J.K. Olson, J. A. Smith. 2012. Endoplasmic reticulum stress regulates the innate immunity critical transcription factor interferon regulatory factor 3. J. Immunol.189:4630-4369. PMID:23028052.
- Spanier, J.A.,F.E. Nashold, J.K. Olson, and C.E. Hayes. 2012. IFN? gene is essential for VDR gene expression and vitamin D3 mediated reduction of the pathogenic T cell burden in the central nervous system in experimental autoimmune encephalomyelitis, a multiple sclerosis model. J. Immunol. 189(6):3188-97.
- Schomberg. D. and J.K. Olson. 2011. Immune responses of microglia in the spinal cord: Contribution to pain states.Exp. Neurology.234:262-270.
- Liu, Y., D.B. Kintner, V. Chanana, X. Chen, J. Algharabli, P. Ferrazzano, J.K. Olson, D. Sun. 2010. Activation of microglia depends on Na+/H+ exchange-mediated H+ homeostasis. J. Neurosci. 30:15210-15220.
- Olson, J.K. 2010. Immune response by microglia in the spinal cord. Ann. N.Y. Acad. Sci. 1198:271-278.
- Bowen, J.L. and J.K. Olson. 2009. Innate immune CD11b+Gr-1+ cells, suppressor cells, affect the immune response during Theiler’s virus- induced demyelinating disease. J. Immunol. 183:6971-6980.
- Olson, J.K. and S.D. Miller. 2009. The innate immune response affects the development of the autoimmune response in Theiler’s virus- induced demyelinating disease. J. Immunol.182:5712-5722.
- Olson, J.K., J.L. Croxford, H.A. Anger, and S.D. Miller. 2005. Initiation and exacerbation of autoimmune demyelination of the central nervous system via virus-induced molecular mimicry: implications for the pathogenesis of multiple sclerosis. J. Virol. 79: 8581-90.
- Olson, J.K., Ercolini A., and S.D. Miller. 2005. A virus-induced molecular mimicry model of multiple sclerosis. Curr Top Microbiol and Immunol. 296:39-53.
- Olson, J.K. and S.D. Miller. 2004. Activation through toll-like receptors leads to antigen presentation by microglia. J. Immunol. 15 :3916-24.
- Olson, J.K., J.L. Croxford, and S.D. Miller. 2004. Innate and adaptive immune requirements for induction of autoimmune demyelinating disease by molecular mimicry. Mol. Immunol. 40: 1103-1108.