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Jessica Hamerman, Ph.D.
Jessica Hamerman, Ph.D.
Associate Member, Benaroya Research Institute and Affiliate Associate Professor, Immunology
Jessica Hamerman received her B.S. in Biological Sciences from Stanford University and her Ph.D. in Immunology from the University of Washington. She then pursued postdoctoral studies at the University of California San Francisco before joining the Benaroya Research Institute Immunology Program.
Benaroya Research Institute at Virginia Mason
1201 Ninth Avenue
Seattle, WA 98101-2795
Research in our laboratory focuses on the regulation of the innate immune response to pathogens with an emphasis on macrophages and dendritic cells. Macrophages and dendritic cells are distributed throughout the body where they are poised to detect pathogens and to subsequently alert the immune system to the presence of infection through the production of inflammatory mediators. The production of inflammatory mediators, such as tumor necrosis factor (TNF) and other pro-inflammatory cytokines, is tightly regulated. Although these important cytokines are beneficial to the host for pathogen clearance, they can be detrimental if unchecked. This can be seen in septic shock as well as in autoimmune disorders such as rheumatoid arthritis and systemic lupus erythematosus.
Macrophages and dendritic cells recognize pathogens by a variety of cell surface and intracellular receptors including the family of Toll-like receptors (TLR). We study how signaling through pattern recognition receptors results in the appropriate inflammatory response by macrophages and dendritic cells. We are particularly interested in proteins that inhibit signaling through pattern recognition receptors, providing an essential brake to the inflammatory response. We study a variety of cell surface receptors and signaling molecules that regulate TLR responses. Our studies span signal transduction and functional assays of macrophages and dendritic cells in vitro to in vivo infection models and models of autoimmunity. We also are investigating the effect of human autoimmunity susceptibility alleles on macrophage function to test the hypothesis that increased innate immune responses can participate in the predisposition to autoimmune disease. Overall, our goal is to understand how the appropriate inflammatory response is determined to fight against infections, yet protect against autoimmunity.
1. Sun X., Wiedeman A., Agrawal N., Teal T.H., Tanaka L., Hudkins K.L., Alpers C.E., Bolland S., Buechler M.B., Hamerman J.A., Ledbetter J.A., Liggitt D., Elkon K.B. 'Increased ribonuclease expression reduces inflammation and prolongs survival in TLR7 transgenic mice' J Immunol. 2013 Mar 15;190(6):2536-43
2. Yee N.K., Hamerman, J.A. 'ß(2) integrins inhibit TLR responses by regulating ND-kB pathway and p38 MAPK activation' Eur J Immunol. 2013 Mar;43(3):779-92
3. Buechler M.B., Teal T.H., Elkon K.B., Hamerman, J.A. 'Cutting edge: Type 1 IFN drives emergency myelopoiesis and peripheral myeloid expansion during chronic TLR7 signaling' J Immunol. 2013 Feb 1;190(3):886-91
4. Ito H., Hamerman, J.A. 'TREM-2, triggering receptor expressed on myeloid cell-2, negatively regulates TLR responses in dendritic cells' Eur J Immunol. 2012 Jan;42(1):176-85
5. Koth L.L., Cambier C.J., Ellwanger A., Solon M., Hou L., Lanier L.L., Abram C.L., Hamerman J.A., Woodruff P.G. 'DAP12 is required for macrophage recruitment to the lung in response to cigarette smoke and chemotaxis toward CCL2' J Immunol. 2010 Jun 1;184(11):6522-8
B.S., Biological Sciences, Stanford University
Ph.D., Immunology, University of Washington