Michael J. Bevan, Ph.D. , F.R.S.
Investigator, Howard Hughes Medical Institute and Professor, Immunology

Department of Immunology
University of Washington
Office I 604 H HSC, Box 357370
1959 NE Pacific Street
Seattle, WA 98195-7650
Tel: 206.685-3610
Fax: 206.685-3612
Email: mbevan@u.washington.edu

Bevan Lab Members

Dr. Bevan's HHMI web page

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.

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.

Students currently training in the Bevan Lab: Jilian Sacks.

Recent publications:

Urdahl, K.B., J.C. Sun, and M.J. Bevan. (2002). Positive selection of MHC class Ib-restricted CD8+ T cells on hematopoietic cells. Nat. Immunol. 3:772-779.

Sun, J.C. and M.J. Bevan. (2003). Defective CD8 memory following an acute infection without CD4 help. Science 300:339-342.

He, Y.-W., H. Li, J. Zhang, C.-L. Hsu, E. Lin, N. Zhang, J. Guo, K.A. Forbush, and M. J. Bevan. (2004). The extracellular matrix protein mindin is a pattern-recognition molecule for microbial pathogens. Nat. Immunol. 5:88-97.

Tyznik, A.J., J.C. Sun, and M.J. Bevan. (2004). The CD8 population in CD4-deficient mice is heavily contaminated with MHC class II-restricted T cells. J. Exp. Med. 199:559-565.

Sun, J.C., M.A. Williams and M.J. Bevan. (2004). CD4+ T cells are required for maintenance, not programming, of CD8+ memory T cells after acute infection. Nat. Immunol. 5:927-933.

Zehn, D. and M.J. Bevan. (2006). T cells with low avidity for a tissue restricted antigen routinely evade central and peripheral tolerance and cause autoimmunity. Immunity 25:261-270.

Prlic, M., G. Hernandez-Hoyos, and M.J. Bevan. (2006). Duration of the initial TCR stimulus controls the magnitude but not functionality of the CD8+ T cell response. J. Exp. Med. 203:2135-2143.

Williams, M.A., A.J. Tyznik, and M.J. Bevan. (2006). IL-2 signals during priming are required for secondary expansion of CD8+ memory T cells. Nature 441:890-893.

Williams, M.A., Ravkov, E.V. and M.J. Bevan. (2008). Rapid culling of the CD4+ T cell repertoire in the transition from effector to memory. Immunity. 2008 Apr;28(4):533-45.

Zehn, D.S., S.Y. Lee and M.J. Bevan. (209). Complete but curtailed T-cell response to very low-affility antigen. Nature 458:211-214.

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Updated 8/19/09