Pamela J. Fink, Ph.D.
Professor, Immunology

Department of Immunology
University of Washington
Office: I-607H HSC, Box 357650
1959 NE Pacific Street
Seattle, WA 98195-7650
Tel: (206) 685-3608
Fax: (206) 685-3612
Email: pfink@u.washington.edu

Fink Lab Members

Dr. Fink graduated with a B.S. from Indiana University and received her Ph.D. in Biology from Massachusetts Institute of Technology in 1981. Her postdoctoral training was at Stanford University School of Medicine and the University of California, San Diego. She joined the University of Washington faculty in 1990.

There are currently three areas of study in the Fink laboratory. First, a line of TCR Vß5 transgenic mice has been used to study the induction of self tolerance among mature peripheral T cells. An age-dependent deletion of populations of transgenic T cells results from encounter with a self antigen. Upon recognition of the tolerogen, T cells undergo both phenotypic and functional changes prior to their deletion. CD8+ T cells that are marked for deletion enter a distinct CD8low Vß5low compartment of deletional intermediates. CD4+ T cells in these animals are driven by the tolerogen to reexpress the recombination machinery (including RAG genes), resulting in rearrangement and expression of endogenous TCRß chain genes. Current work is focused on understanding the mechanism of TCR revision, the process of inducing tolerance through expression of alternate TCRs. The second line of research is focused on the ability of Fas ligand to deliver a positive reverse signal to maximize the antigen specific proliferation of Fas ligand-expressing CD8+ T cells. Fas ligand bipolar signaling functions in vivo to double or triple the burst size of responding cytolytic T cells. Signaling through Fas ligand also influences the maturation of thymocytes bearing TCRs of moderate affinity. The mechanism of reverse signaling through Fas ligand is under current investigation. The third area of study is the analysis of recent thymic emigrants from mice carrying a transgene for green fluorescent protein driven by the RAG2 promoter. T cells complete both functional and phenotypic maturation in the lymphoid periphery, and current investigation centers on the signals provided by the peripheral environment that promote this post-thymic phase of T cell maturation.

Students currently training in the Fink Lab: Mingyi Sun, J. Scott Hale, Evan Houston, and Deborah Hendricks

Some recent publications:

Fink, P.J. and C.J. McMahan. (2000). Lymphocytes rearrange, edit, and revise their antigen receptors to be useful yet safe. Immunol. Today, 27:561-566.

Cooper, C.J., M.T. Orr, C.J. McMahan, and P.J. Fink. (2003). T cell receptor revision does not solely target recent thymic emigrants. J. Immunol. 171:226-233.

Boursalian, T.E. and P.J. Fink. (2003). Mutation in Fas ligand impairs maturation of thymocytes bearing moderate affinity T cell receptors. J. Exp. Med. 198:349-360.

Boursalian, T.E., J. Golob, D.M. Soper C.J. Cooper and P.J. Fink. (2004). Continued maturation of thymic emigrants in the periphery. Nature Immunol. 5:418-425.

Cooper, C.J., G. Turk, M. Sun, A.G. Farr, and P.J. Fink. (2004). Cutting Edge: TCR revision occurs in germinal centers. J. Immunol. 173:632-6536.

Hale, J.S., T.E. Boursalian, G.L. Turk, and P.J. Fink. 2006. Thymic output in aged mice. Proc. Natl. Acad. Sci. USA: 103:8447-8452.

Sun, M., K.T. Ames, I. Suzuki, and P.J. Fink. 2006. The cytoplasmic domain of Fas ligand costimulates TCR signals. J. Immunol.: 177:1481-1491.

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Updated 7/5/2007