Eugene C. Butcher

Eugene C. Butcher
Born (1950-01-06) January 6, 1950
Citizenship American
Nationality United States
Fields Immunology
Institutions Stanford University
Alma mater
Notable awards

Eugene C. "Gene" Butcher, M.D. (born 6 January 1950) is an immunologist and a Professor of Pathology at Stanford University [1]

Career

Eugene Butcher gained an undergraduate degree in chemistry from Massachusetts Institute of Technology in Boston and an MD from Washington University in St. Louis. In 1976 he began a residency in pathology at Stanford University in California, and was awarded a professorship in the Department of Pathology there. He is also staff physician and Director of the Serology and Immunology Section at the Veterans Administration, Palo Alto Health Care System.[2]

Research focus

Butcher and his research team study the trafficking of white blood cells (lymphocytes, dendritic cells, monocytes, etc.), including their interactions with the endothelial lining of blood vessels at sites of leukocyte extravasation, and their chemotactic responses in tissues. These events regulate immune responses by controlling the access of leukocytes to sites of inflammatory or immune reaction in the body. He and his research team have shown that lymphocytes use a variety of different adhesion molecules or "homing receptors" to recognize organ (and/or inflammation)-specific vascular ligands or "addressins" that define the tissue position (address) of blood vessels in the body. Their studies have shown that these adhesion receptors act coordinately with G protein-linked serpentine chemoattractant receptors in a multi-step process that controls the specificity and provides combinatorial diversity in leukocyte trafficking.[3]

A major focus of the group is on understanding the physiologic significance and control of targeted lymphocyte trafficking. To this end, they are studying the specialized homing mechanisms and functional properties of tissue infiltrating lymphocytes involved in local immune, autoimmune and regulatory responses in the GI tract (intestines, liver), skin, lungs, and other sites. Genetic, antibody and small molecule-based approaches allow them to define the role of trafficking molecules and mechanisms in models of autoimmune and infectious diseases. The team is also exploring mechanisms that imprint lymphocyte homing and chemokine receptor expression during tissue-specific immune responses, and are developing techniques to recapitulate such regulation in vitro for cell targeting and therapy. Dendritic cells (DC) play an important role in this context, and they are interested in the mechanisms by which specialized DC “interpret” and process local environmental signals (e.g. vitamins, metabolites, cytokines) to control T cell trafficking and regulatory vs. effector activities.[3]

In other investigations, the team has identified novel lymphocyte, dendritic cell and macrophage chemoattractants and receptors, as well as monocyte and arterial wall endothelial molecules that regulate monocyte-endothelial interactions in models of atherogenesis. They are interested in the structure and function of these molecules, and their importance in disease models. Finally, they have shown that leukocytes can effectively navigate through complex chemoattractant arrays, and they are exploring the mechanisms that permit this surprising behavior through computer simulations of chemotactic behavior, and through experimental manipulation of the molecules and receptors involved.[3]

Recent Publications

Awards

Crafoord Prize awarded by the Royal Swedish Academy of Sciences, 2004

References

This article is issued from Wikipedia - version of the 7/27/2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.