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Joseph C. Fantone, M.D. |
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Annual Report | Biography | Clinical Interests | Research Interests
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Departmental Annual Report |
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Brief Biography Dr. Fantone earned his M.D. degree from the University of Connecticut in 1977, following which he served as a resident in anatomic pathology at the National Institutes of Health. He then returned to the University of Connecticut for a postdoctoral fellowship in immunopathology from 1979-80. In 1980, Dr. Fantone joined the faculty of the University of Michigan as an Instructor in Pathology, after which he was promoted in 1986 to Associate Professor of Pathology and Professor of Pathology in 1991.In addition to his research and teaching activities in the Department of Pathology, Dr. Fantone has been actively involved in the administrative and educational programs of the Medical School, as Component I and II Director and was appointed Associate Dean for Medical Education in January, 1998. He has overall responsibility for the undergraduate medical school curriculum and the several operational/administrative issues associated with that curriculum.
Clinical Interests Pathology, Immunopathology and pulmonary pathology.
Research Interests Inflammation-cell activation and mechanisms of tissue
injury. The primary research activities in our laboratory focus on the investigation of the cellular and biochemical mechanisms involved in the regulation of phagocytic cell activation. Phagocytic cells include polymorphonuclear leukocytes and monocytes which circulate in blood, as well as macrophages present in most tissues of the body. These cells play an important role in the host defense against infection and as central participants in both immunologic and inflammatory responses. Currently, we are attempting to define the signal translation mechanisms involved in polymorphonuclear leukocyte activation via two distinct receptor systems: Fcg receptors and leukocyte adhesion molecules. Additional areas of study include investigation of the pathogenesis of legionella pneumophila lung infection and mechanisms of myocardial ischemic-reperfusion injury.
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