Professional Bio
David G. Harrison, MD, FACC, FAHA, Professor of Medicine in the Department of Medicine at Vanderbilt University Medical Center. His research laboratory has been focused on understanding how inflammation, and in particular, the adaptive immune response contributes to hypertension.
His lab found that T cells are essential for the development of hypertension and has shown that various hypertensive stimuli, including angiotensin II, norepinephrine and DOCA-salt cause activation of T cells and leads to their accumulation in the perivascular fat and kidneys. The data indicates that T cell-derived cytokines such as IL-17 and TNF-a enhance vasoconstriction and sodium retention, leading to the hypertensive phenotype. Central signals derived from the circumventricular organs contribute to T cell activation, and manipulation of signals from this region affect T cell activation and the eventual elevation in blood pressure caused by angiotensin II.
Dr. Harrison's lab is studying mechanisms involved in T cell activation in response to hypertensive stimuli. They have recently shown that gamma-ketoaldehydes, or isolevuglandins (isoLGs) adduct to proteins in hypertensive mice and humans, and that these are immunogenic. These modified proteins seem to act as 'auto-antigens' that promote dendritic cell and ultimately T cell activation in hypertension. Recent studies have defined characteristics of class I major histocompatibility complexes that accommodate isoLG adducted peptides, leading to identification of several candidate renal derived peptides that act as antigens in hypertension.
Publications
Education
MD - Oklahoma State University, 1974
Internship - Duke University, 1975
Residency - Duke University, 1977
Fellowship - CA - University of Iowa, 1982
Contact
Email
Kimryn.Rathmell@Vumc.Org
Address
777 Preston Research Building
2220 Pierce Ave
Nashville, TN 37232-6307