Dr. Freedman is an Associate Professor in the Department of Pharmacology. She is also affiliated with the Center for Immunology, Masonic Cancer Center, and Center for Autoimmune Diseases Research at UMN. She completed her AB with honors in Biochemistry at Bowdoin College in Brunswick, Maine, and her PhD in Molecular and Cell Biology at the University of California, Berkeley, studying the structural biology of Ras-activating proteins. She completed her postdoctoral fellowship at the University of California, San Francisco, where she discovered a mechanism by which the Src-family kinase LynA tunes macrophage sensitivity to pro-inflammatory activation, a process with implications for myeloid-cell hypersensitization in autoimmune disease.
The Freedman lab studies mechanisms by which myeloid cells and lymphocytes integrate positive- and negative-regulatory signals to achieve tissue-specific functions and drive pathologies from autoimmune disease (e.g., lupus/SLE, inflammatory arthritis/RA/JIA) to breast cancer. Immune-cell responses are triggered by complex networks of signaling pathways that intersect and feed back for higher-order regulation. The effectiveness of this regulatory control is the key difference between an appropriate antimicrobial response and chronic inflammation or immunosuppression. The lab investigates how cells discriminate between different types of extracellular molecules, how cells achieve tissue-specific functions, and how immune responses become dysregulated in disease. Mechanisms regulated by tyrosine kinases (e.g., Src homologs LynA and LynB) and phosphatases (e.g., PTPN22, SHP-1) in myeloid cells such as macrophages, dendritic cells, and mast cells, are areas of particular interest to the lab.
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