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Department of Immunology Dr. Goverman received a Bachelors degree in Chemistry from Brandeis University. She received a Ph.D. in Biological Chemistry from the University of California, Los Angeles in 1981. A postdoctoral fellowship at UCLA was followed by additional training at the California Institute of Technology. A member of the Department of Molecular Biotechnology when it was founded at the University of Washington in 1992, Dr. Goverman joined the Department of Immunology in 1994. Dr. Goverman's research focuses on the pathogenesis of autoimmune disease. Autoimmunity is believed to arise from a breakdown in tolerance to self-antigens. Multiple sclerosis (MS) is an autoimmune disease in which self-reactive T cells target myelin proteins in the central nervous system (CNS). The research program focuses on defining mechanisms that maintain immune tolerance to myelin proteins, determining triggers that break this tolerance, and elucidating how myelin-specific T cells mediate disease. We are interested in the precise mechanisms by which myelin-specific T and B cells contribute to autoimmunity in the CNS, and the role of regulatory T cells in suppressing this disease. With these objectives in mind, we have engineered a number of animal models using T cell receptor transgenic mice that express either CD4+ or CD8+ T cell receptors specific for myelin basic protein. These models have revealed novel mechanisms of tolerance induction, as well as generated experimental systems that recapitulate more faithfully the complex pathology seen in MS patients. Our models uniquely position us to investigate the contribution of both CD4+ and CD8+ T cells to autoimmunity in the CNS, to define the parameters that govern T cell trafficking in the CNS, and to study the effector mechanisms that mediate this inflammatory, demyelinating disease. Our long-term goal is to further our understanding of the pathogenesis of MS in order to define potential targets for therapeutic intervention. Selected publications from Ph.D. students in the Goverman laboratory: Harrington, C., A. Paez, T. Hunkapiller, V. Mannikko, M. Ahern, C. Besson, J. Goverman. 1998. Differential Tolerance is Induced in T Cells Recognizing Distinct Epitopes of Myelin Basic Protein. Immunity 8:571-580.
Brabb, T., P. Von Dassow , N. Ordonez, B. Schnabel, B. Duke, and J. Goverman. 2000. In-Situ Tolerance Within the CNS as a Mechanism for Preventing Autoimmunity. J. Exp. Med. 192:871-880.
Huseby, E.S., B. Sather, P.G. Huseby and J. Goverman. 2001. Age -Dependent T Cell Tolerance and Autoimmunity to Myelin Basic Protein. Immunity 14:471-481.
Huseby, E.S., D. Liggitt, T. Brabb, B. Schnabel, C. Ohlen and J. Goverman. 2001. A Pathogenic Role for Myelin-Specific CD8+ T Cells in a Model for Multiple Sclerosis. J. Exp. Med. 194:669-676.
Seamons, A., Sutton, J., Bai D., Baird. E., Bonn, N., Kafsack, B.F.C., Shabanowitz, J., Hunt, D.F., Beeson, C. and J. Goverman. 2003. Competition Between Two MHC Binding Registers in a Single Peptide Processed From Myelin Basic Protein Influences Tolerance and Susceptibility to Autoimmunity. J. Exp. Med. 197:1391-7.
Perchellet, A., Stromnes, I., Pang J. and J. Goverman. 2004. CD8+ T Cells Maintain Tolerance to Myelin Basic Protein by Epitope Theft. Nature Immunology 5:606-614.
Seamons, A, Perchellet, A. and J. Goverman. 2006. Endogenous Myelin Basic Protein Is Presented in the Periphery by Both Dendritic Cells and Resting B Cells With Different Functional Consequences. J. Immunology 177: 2097-2106.
Cabbage, S., Huseby, E.S., Sather, B., Brabb, T. D. Liggitt and J Goverman. 2007. Regulatory T cells maintain long-term tolerance to myelin basic protein by inducing a novel, dynamic state of T cell tolerance. J. Immunol., 178:887-896.
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Updated 7/5/07
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