Robert B. Fritz, PhD
Professor
Microbiology and Molecular Genetics
Medical College of Wisconsin
Research Focus: Cellular Immunology, Experimental Autoimmunity
PhD: Duke University (1967) Immunology |
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The focus of my research is the basic immunobiology of experimental autoimmune disease, in particular, experimental allergic encephalomyelitis (EAE). EAE is used as a model for the human disease, multiple sclerosis, due to clinical and histopathological similarities. EAE is induced in susceptible strains of animals by immunization with myelin proteins isolated from autologous central nervous system tissue. In mice the disease presents as relapsing, remitting paralysis with significant central nervous system pathology. The disease process is mediated primarily, if not solely, by neuroantigen-specific T lymphocytes. Current research projects include analysis of infiltration of encephalitogenic T cells into the central nervous system, and identification and characterization of cells involved in regulation of the encephalitogenic response. Using transgenic mice and mice in which genes important for immune function have been inactivated, NK1.1+ cells have been identified as important for modulation of the immune response to self-antigens. Studies are in progress to characterize the regulatory cells further, and to investigate the mechanism of regulation.
Recent Publications
Baldwin MR, Tepp WH, Pier CL, Bradshaw M, Ho M, Wilson BA, Fritz RB, Johnson EA, Barbieri JT. Characterization of the antibody response to the receptor binding domain of botulinum neurotoxin serotypes A and E. Infect Immun. 2005 Oct;73(10):6998-7005.
Abstract
Sewell DL, Reinke EK, Co DO, Hogan LH, Fritz RB, Sandor M, Fabry Z. Infection with Mycobacterium bovis BCG diverts traffic of myelin oligodendroglial glycoprotein autoantigen-specific T cells away from the central nervous system and ameliorates experimental autoimmune encephalomyelitis. Clin Diagn Lab Immunol. 2003 Jul;10(4):564-72.
Abstract
Fritz RB, Zhao ML. Regulation of experimental autoimmune encephalomyelitis in the C57BL/6J mouse by NK1.1+, DX5+, alpha beta+ T cells. J Immunol. 2001 Mar 15;166(6):4209-15.
Abstract
Fritz RB, Wang X, Zhao ML. Alterations in the spinal cord T cell repertoire during relapsing experimental autoimmune encephalomyelitis. J Immunol. 2000 Jun 15;164(12):6662-8.
Abstract
Fritz RB, Wang X, Zhao ML. The fate of adoptively transferred quiescent encephalitogenic T cells in normal and antigen-tolerized mice. J Neuroimmunol. 2000 Jul 10;107(1):66-72.
Abstract
Lyons JA, Zhao ML, Fritz RB. Pathogenesis of acute passive murine encephalomyelitis II. Th1 phenotype of the inducing population is not sufficient to cause disease. J Neuroimmunol. 1999 Jan 1;93(1-2):26-36.
Abstract
Contact Information
Email: rfritz@mcw.edu
Phone: 414-456-8414
Room: BSB-207