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Pamela J. Fink, Ph.D.
Pamela J. Fink, Ph.D.
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.
Department of Immunology
University of Washington
Office E-471, Box 358059
750 Republican St.
Seattle WA 98109-8059
There are currently two 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 re-express 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 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 and on the details of the observed functional defects. We are interested in understanding the purpose of this transitional phase, and suspect that recent thymic emigrants are more easily tolerized than their mature counterparts, a hypothesis we are testing in infectious disease, diabetes, and colitis model systems.
1. Simmons, K.B.1, M. Wubeshet1, K.T. Ames, C.J. McMahan, J.S. Hale, and P.J. Fink. 2012. Modulation of TCRbeta surface expression during TCR revision. (1: authors contributed equally) Cell. Immunol. 272:124-129. PMCID: PMC3244515
2. Houston, E.G. Jr., T.E. Boursalian, and P.J. Fink. 2012. Homeostatic signals do not drive post-thymic T cell maturation. Cell. Immunol. 274:39-45. PMCID: PMC3334402
3. Martins, V., E. Ruggiero, S.M. Schlenner, V. Madan, M. Schmidt, P.J. Fink, C. von Kalle, and H.R. Rodewald. 2012. Thymus-autonomous T cell development in the absence of progenitor import. J. Exp. Med. 209:1409-1417. PMCID: PMC3420332
4. Fink, P.J. 2013. The biology of recent thymic emigrants. Annu. Rev. Immunol. 31:31-50.
5. Vanden Driessche, K., A. Persson, B.J. Marais, P.J. Fink, and K.B. Urdahl. 2013. Immune vulnerability of infants to tuberculosis. Clin. Devel. Immunol. Article ID 781320; http://dx.doi.org/10.1155/2013/781320
6. Fink, P.J. 2013. Working to fill the Boss’s shoes. J. Immunol. 191:1-2.
7. Berkley, A.M.1, D.W. Hendricks1, K.B. Simmons, and P.J. Fink. 2013. Recent thymic emigrants and mature naïve T cells exhibit differential DNA methylation at key cytokine loci. (1: authors contributed equally) J. Immunol. 190:6180-6186. NIHMS 473235
8. O’Leary, M.N., K.H. Schreiber, Y. Zhang, A.C.E. Duc, S. Rao, J.S. Hale, E.C. Academia, S.R. Shah, J.F. Morton, C.A. Holstein, D.B. Martin, M. Kaeberlein, W.C. Ladiges, P.J. Fink, V.L. MacKay, D.L. Wiest, and B.K. Kennedy. 2013. The ribosomal protein Rpl22 controls ribosome composition by directly repressing expression of its own paralog, Rpl22l1. PLoS Genetics 9:e1003708. doi:10.1371/journal.pgen.1003708
B.S., Biological Sciences, Indiana University
Ph.D., Biology, Massachusetts Institute of Technology