Michael J. Bevan, Ph.D., F.R.S.

Michael J. Bevan, Ph.D., F.R.S.

Professor, Immunology and Howard Hughes Medical Institute Investigator

Dr. Bevan received his Ph.D. in Immunology at The National Institute for Medical Research int Mill Hill, London, in 1972. Prior to joining the University of Washington in 1990, he held positions at Scripps Research Institute in La Jolla, California, the Massachusetts Institute of Technology,and The Salk Institute. He is a Howard Hughes Medical Institute Investigator and a Fellow of the Royal Society of London, and a member of the U.S. National Academy of Sciences.

Contact Info

Department of Immunology
University of Washington  
Office E441, Box 358059
750 Republican Street
Seattle WA 98109-8059
Phone: 206-685-3610
Fax: 206-685-3612

Research Areas

  • Adaptive Immune Responses
    Infectious Diseases



Click here to view publication list

T lymphocytes mature in the thymus and recognize "processed" forms of antigens presented by major histocompatibility complex-encoded molecules. Dr. Bevan's laboratory studies CD8+ cytotoxic T lymphocytes (CTL) which recognize peptide fragments of proteins of viral or bacterial origin bound by class I MHC molecules. The goal of experiments in the Bevan laboratory is a detailed description of how cytotoxic T cells mature, how the responses to foreign antigen is regulated, the processes whereby these antigens are presented in vivo, and how long-lived protective memory to pathogens is achieved. In response to pathogen infection, CD8+ cells can go through 15 or more cell divisions within 6 days to generate millions of cytotoxic effectors. When the infection is cleared, 90-99% of effectors die leaving a pool of long-lived memory cells with stem cell-like properties. Our lab studies many aspects of this process of expansion, contraction and memory formation. We also study those peripheral T cells which recognize self antigen with a low affinity but which can cause autoimmunity, such as diabetes, when they are activated by a pathogen which carries a cross-reactive antigen. The lab is also investigating the immune response to the neuroinvasive pathogen, West Nile Virus.

1. Mehlhop-Williams, E.R. and M.J. Bevan (2014) Memory CD8+ T cells exhibit increased antigen threshold requirements for recall proliferation. J. Ep. Med. in press.

2. Zhang, N. and M.J. Bevan (2013) TGF-β signaling controls the formation and maintenance of gut-resident memory T cells through distinct mechanisms. Immunity 39: 687-696.

3. Murphy, S.C., A. Kas, B.C. Stone and M.J. Bevan (2013)  A T cell response to a liver-stage Plasmodium antigen is not boosted by repeated sporozoite immunizations. Proc. Natl. Acad. Sci. USA 110:  6055-6060.

4. Zhang, N. and M. J. Bevan (2012) TGF-β signaling to T cells inhibits autoimmunity during lymphopenia-driven proliferation. Nat. Immunol. 13: 668-673. PMID: 22634866

5. Zhang, N. and M.J. Bevan (2011) Foot soldiers of the immune system.  Immunity 35: 161-168. PMID: 21867926

6. Wakim, L.M., A. Woodward-Davis and M. J. Bevan (2010) Memory T cells persisting within the brain after local infection show functional adaptations to their tissue of residence. Proc. Natl. Acad. Sci. USA, 107: 17872-17879.  PMID:20923878

7. Zhang, N. and M. J. Bevan (2010) Dicer controls CD8+ T-cell activation, migration, and survival. Proc. Natl. Acad. Sci. USA, 107: 21629-21634.  PMID:21098294

8. Bevan, M. J. (2011) Memory T cells as an occupying force. Europ. J. Immunol. 41: 1192-1195. PMID: 21469134

9. Bevan, M. J. (2011) Understand memory, design better vaccines. Nat. Immunol. 12:463-465. PMID: 21587308

10. Wakim, L. M. and M. J. Bevan (2011) Cross-dressed dendritic cells drive memory CD8+ T-cell activation after viral infection. Nature 471: 629-632. PMID: 21455179

B.Sc., Zoology, University College, London
M.Sc., Biochemistry, University College, London
Ph.D.,  The National Institute for Medical Research, Mill Hill, London

Postdoctoral Fellows
Tessa Bergsbaken, bergst@uw.edu
Amanda Woodward-Davis, aswdawg@uw.edu