Barbara A. Osborne
My laboratory focuses on the differentiation and function of mature CD4+ lymphocytes. In particular, we are interested in the role of Notch proteins in CD4+ maturation and function.
Over the past several years, we have demonstrated that Notch plays a critical role in the differentiation of the T-helper 1 (Th1) and T-helper17 (Th17) subsets of T cells. Both Th1 and Th17 cells have been implicated in several diseases including experimental autoimmune encephalomyelitis (EAE), a mouse model of Multiple Sclerosis. Using gamma-secretase inhibitors (GSIs), compounds that block the activation of Notch, we have found that we can block the development of EAE in mice, suggesting that GSIs may be a possible therapeutic for the treatment of MS. Our current studies are focused on determining how Notch signaling influences the development of EAE as well as determining which Notch family member is important in the development of disease. In mammals, there are four Notch family members and it is unclear which Notch family member is most important in driving EAE. Additionally, in collaboration with our colleagues in the Center for Bioactive Delivery, we are actively engaged in developing tools that will allow us to selectively inhibit Notch signaling in potentially pathogenic T cells.
Learn more at www.vasci.umass.edu/research-faculty/barbara-a-osborne
- BA, English, Moravian College, 1970
- PhD, Genetic & Immunology, Stanford University Medical School, 1979
- Damon Runyon Postdoctoral fellow, National Institutes of Health, 1979-83