Cynthia L. Baldwin
Professor of Virologoy & Microbiology, University of Massachusetts
Ph.D.: Cornell University, Immunology, 1983 Postdoctoral Training: International Laboratory for Research on Animal Diseases, Nairobi, Kenya
While macrophages are normally considered to be a primary cell for mediating innate immune responses by phagocytosing and destroying microbes that infect mammals, some microbial organisms including bacteria and protozoa have specifically adapted themselves to survive and replicate in host cells thereby "hiding" from protective immune responses. We study Brucella abortus, a bacterium that causes disease in a wide variety of agricultural animals and in people, to evaluate how some animals but not others successfully prevent infections by intracellular pathogens. We are particularly interested in the role of host cytokines such as interleukins and gamma-interferon produced by T lymphocytes in controlling the infection through their ability to activate macrophages for antimicrobial activities. In addition we are interested in identifying genes of the bacteria that facilitate their survival in host macrophages thus allowing them to establish chronic infections. Our second major area of research evaluates gamma delta T cells, a subpopulation of T lymphocytes that comprise a major proportion of lymphocytes in mammals but whose role in mediating protective immunity is unclear at this time. We are studying how this subpopulation of T lymphocytes is activated by constitutively expressed molecules on macrophages and the ability of a killed leptospira vaccine to prime gamma delta T cells for recall responses to leptospira components. We are also interested in the role a lineage-specific cell-surface molecule of gamma delta T cells, known as WC1, plays in signal transduction and activation of these cells and understanding why expression of particular isoforms of WC1 correlates with functional differences of the T cells.