Pamela J. Fink, Ph.D.

Pamela J. Fink, Ph.D.

Professor, Immunology

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.  Dr. Fink is the current Editor-in-Chief of The Journal of Immunology, the flagship journal of The American Association of Immunologists.

Contact Info

Department of Immunology
University of Washington  
Office E-471, Box 358059
750 Republican St.
Seattle WA 98109-8059
Phone: 206-897-1715
Fax: 206-616-4274

Research Areas

  • Adaptive Immune Responses
    Developmental Immunology
    Tolerance & Autoimmunity

LAB

Pubmed

Pamela J. Fink

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, through either deletion or replacement of the self-reactive TCR by a novel process called TCR revision.  In this latter pathway, CD4+ T cells are driven by the tolerogen to re-express the recombination machinery (including RAG genes), resulting in rearrangement and expression of endogenous TCRß chain genes.  Recent work has localized this process to the germinal centers, and the focus now is on understanding the impact of TCR revision on B cells and determining whether revision occurs in TCR nontransgenic mice. 

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, a process driven by factors other than those that control T cell homeostasis and survival.  We are interested in understanding the purpose of post-thymic T cell maturation, and current work centers on using a diabetes model system to test the hypothesis that recent thymic emigrants are more invasive yet more easily tolerized than their mature counterparts. 


1.  Hendricks, D.W. and P.J. Fink. 2011. Recent thymic emigrants are biased against the Th1 and toward the Th2 effector lineage.  Blood 117:139-1249. PMCID: PMC3056472

2.  Hale, J.S., L.T. Nelson, K.B. Simmons, and P.J. Fink.  2011.  Bcl-2-interacting mediator of cell death influences autoantigen-driven deletion and TCR revision.  J. Immunol. 186:799-06.  PMCID: PMC3233758

3. Houston, E.G., Jr., L.E. Higdon, and P.J. Fink. 2011.  Recent thymic emigrants are preferentially incorporated only into the depleted T-cell pool. Proc. Natl. Acad. Sci USA 108:5366-5371. PMCID: PMC3069187

4. Fink, P.J. and D.W. Hendricks. 2011. Post-thymic maturation: young T cells assert their individuality. Nature Rev. Immunol. 11:544-549. PMCID: PMC3241610

5.     Simmons, K.B.1, M. Wubeshet1, K.T. Ames, C.J. McMahan, J.S. Hale, and P.J. Fink. 2012. Modulation of TCRβ surface expression during TCR revision. (1: authors contributed equally) Cell. Immunol. 272:124-129. PMCID: PMC3244515

6.     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

7.     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

8.     Fink, P.J. 2013. The biology of recent thymic emigrants. Annu. Rev. Immunol. 31:31-50.

9.     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

10.   Fink, P.J. 2013. Working to fill the Boss’s shoes. J. Immunol. 191:1-2.

11.     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. PMCID:  PMC3679312

12.     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

Graduate Students
Amy Berkley, amb25@uw.edu
Travis Friesen, tfriesen@uw.edu

Laboratory Staff
Katie Deets, deetsk@uw.edu
Kayla Vargas, varkay00@uw.edu
Damion Winship, dwinship@gmail.com

Visiting Scientist
Mary Philip,
adastra@uw.edu

Lab at Lake Serene