Department of Immunology

Pamela J. Fink, PhD


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 a former Editor-in-Chief of The Journal of Immunology, the flagship journal of The American Association of Immunologists. Dr. Fink retired from the department in January 2019, and was appointed Professor Emeritus.


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

Fax: 206-221-5433


Adaptive Immune Responses
Tolerance & Autoimmunity
Developmental Immunology


Pamela J. Fink




The Fink Lab focused on the analysis of recent thymic emigrants (the youngest peripheral T cells) from mice carrying a transgene for green fluorescent protein driven by the RAG2 promoter. Our lab has shown that 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. Our findings suggest the purpose of post-thymic T cell maturation is to expose young T cells to antigens expressed only outside the thymus, during a tolerance-prone transitional phase of development. Current work is centered on dissecting the metabolic reprogramming that defines peripheral T cell maturation, interrogating the environmental cues (such as the inflammatory milieu) that tune this tolerance process and developing a model to test the involvement of recent thymic emigrants (including neonatal T cells) in tumor rejection.


  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. Fink, P.J. 2013. The biology of recent thymic emigrants. Annu. Rev. Immunol. 31:31-50.
  6. 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
  7. Higdon, L.E., K.A. Deets, T.J. Friesen, K.Y. Sze, and P.J. Fink. 2014. Receptor revision in CD4 T cells is influenced by follicular helper T cell formation and germinal center interactions. Proc. Natl. Acad. Sci. USA 111:5652-5657.  PMCID: PMC3992682
  8. Berkley, A.M. and P.J. Fink. 2014. Cutting Edge: CD8+ recent thymic emigrants exhibit increased responses to low affinity ligands and improved access to peripheral sites of inflammation.  J. Immunol. 193:3262-3266. PMCID: PMC4170019
  9. Deets. K.A.1, A.M. Berkley1, T. Bergsbaken, and P.J. Fink. 2016. Cutting Edge: Enhanced clonal burst size corrects an otherwise defective memory response by CD8+ recent thymic emigrants. (1: authors contributed equally) J. Immunol. 196:2450-2455. PMCID: PMC4779721
  10. Friesen, T.J., Q. Ji, and P.J. Fink. 2016. Recent thymic emigrants are tolerized in the absence of inflammation. J. Exp. Med. 213:913-920. PMCID: PMC4886366