Dr. Dorothy E. Lewis
The University of Texas Health Science Center at Houston
Department of Internal Medicine - Infectious Diseases
Dr. Lewis is interested in HIV pathogenesis. A major focus is to test the hypothesis that Granzyme B (GrB), a serine protease, mediates gut breach leading to chronic immune activation in HIV. Granzyme B plays a big role in CD8 and NK cell effector function (killing targets) but Dr. Lewis has found that human memory CD4 T cells make and release tissue destructive amounts of GrB. Primates that develop pathogenic SIV infection have large numbers of CD4+ GrB+ cells in the intestinal lamina propria, however, primates that do not develop pathogenesis have much lower numbers of these cells, suggesting a mechanism that prevents pathogenesis in those primate hosts. Her lab is pursuing mechanisms of GrB production and destruction using in vitro and in vivo models.
More than half of all HIV infected people develop metabolic disorders similar to that found in obesity. Dr. Lewis is testing the hypothesis that activated/infected immune cells influence fat metabolism. Dr. Lewis found that soluble molecules (IL-6 and VLA-1 ligands) from preadipocytes and adipocytes induce more T cell activation and HIV production from human memory CD4 T cells. In addition, immune cells block adipocyte differentiation. Both observations may be related to HIV associated changes in metabolism that occur. Her lab has both in vitro and in vivo models to examine how fat and immune cells interact that might enhance HIV pathogenesis/latency.
Types of projects: Human T cell effector function as it relates to intestinal tissue damage and metabolic disorders. Work involves isolation of human T cells, activation, HIV infection, and use of flow cytometry to measure functional aspects.
Office: MSB 5.113
Ph.D. - University of Arizona - 1978