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Andrew G. Farr, Ph.D.
Andrew G. Farr, Ph.D.
Professor, Biological Structure and Immunology
Dr. Farr did his undergraduate work at the University of Colorado in Boulder and received his Ph.D. in Anatomy from the University of Chicago in 1975. He is affiliated with the University of Washington Diabetes Research Center and has been a member of the Department of Biological Structure at the University of Washington since 1982.
Department of Biological Structure
University of Washington
Office I534, HSC, Box 357420
1959 NE Pacific Street
Seattle WA 98195
The efforts of this laboratory are directed at defining the non-lymphoid elements comprising the thymic environment, and gaining a better understanding of their contributions to the production and differentiation of T lymphocytes. A number of approaches are taken, including monoclonal antibody technology to define the phenotypic heterogeneity of the stromal cells comprising the thymic environment and to identify stromal cell surface molecules involved in T-lymphopoiesis. Molecular biological approaches are used to clone genes encoding stromal cell surface molecules and to generate soluble forms of these cell surface molecules as a means to assess their functional significance in vitro and in vivo. Tissue culture approaches are utilized to generate stromal cell lines representative of the different stromal cell populations and to assess their ability to support various aspects of T-lymphopoiesis in vitro. Finally, ultrastructural immunohistochemistry is used to precisely define the expression of cell interaction molecules within the thymic environment.
1. Furuya M, Kirschbaum SB, Paulovich A, Pauli BU, Zhang H, Alexander JS, Farr AG, Ruddell A (Nov 2010) Lymphatic endothelial murine chloride channel calcium-activated 1 is a ligand for leukocyte LFA-1 and Mac-1., Journal of immunology (Baltimore, Md. : 1950), 185 (10), 5769-77
2. Cohen JN, Guidi CJ, Tewalt EF, Qiao H, Rouhani SJ, Ruddell A, Farr AG, Tung KS, Engelhard VH (Apr 2010) Lymph node-resident lymphatic endothelial cells mediate peripheral tolerance via Aire-independent direct antigen presentation., The Journal of experimental medicine, 207 (4), 681-8
3. Dumortier A, Durham AD, Di Piazza M, Vauclair S, Koch U, Ferrand G, Ferrero I, Demehri S, Song LL, Farr AG, Leonard WJ, Kopan R, Miele L, Hohl D, Finke D, Radtke F (2010) Atopic dermatitis-like disease and associated lethal myeloproliferative disorder arise from loss of notch signaling in the murine skin., PloS one, 5 (2), e9258
B.A., University of Colorado, Boulder
Ph.D., Anatomy, University of Chicago