Mark Davis

Mark M. Davis, PhD, Professor, Department of Microbiology and Immunology; Investigator, Howard Hughes Medical Institute; Director, Stanford Institute for Immunity, Transplantation and Infection, Stanford University School of Medicine


Research Description: Dr. Davis has a longstanding interest in lymphocyte recognition and human immune responses. His group identified elements of the T-cell receptor (TCR) and showed the immunoglobulin-like yet distinct character of the TCR. Together with parallel work on the proteins using clonotypic antibodies, this laid the modern foundation for the many subsequent studies of T cell recognition.  His group also developed the peptide-MHC tetramer technique, a gold-standard in the field of immunology and diabetes research. Recently his group has refined and optimized the tetramer technology to understand better how a standard vaccine works. They have also found a surprising complexity of immune responses using emerging CyTOF technology and used it to survey over 100 different tetramers simultaneously. They have also shown that negative selection is not an efficient mechanism of T cell tolerance, and that non-heritable factors, such as virus infections are the dominant influence on immune variables in studies of twins. As director of the Stanford Institute for Immunity, Transplantation and Infection (ITI), Dr. Davis oversees multiple research projects and efforts directly focused on diabetes research, including studies by over 20 members of the SDRC (a subset of investigators with whom he has published studies is listed below). Dr. Davis and the Stanford ITI developed and support the Human Immune Monitoring Center (HIMC) in conjunction with the Center for Clinical Immunology. The Diabetes Immune Monitoring Core in the Stanford DRC is run in the HIMC.


Selected relevant publications (Stanford DRC Members in BOLD):

1.         Newell, E.W., Sigal, N., Bendall, S.C., Nolan, G.P., Davis, M.M. Cytometry by Time-of-Flight Shows Combinatorial Cytokine Expression and Virus-Specific Cell Niches within a Continuum of CD8+ T Cell Phenotypes.  Immunity 36, 142-152, 2012.

2.         Brodin, P., Jojic, V., Gao, T., Bhattacharya, S., Lopez Angel, C.J., Furman, D., Shen-Orr, S., Dekker, C.L., Swan, G.E., Butte, A.J., Maecker, H.T., and Davis, M.M.  Variation in the human immune system is largely driven by non-heritable influences. Cell 160: 37-47, 2015.

3.         Yu, W., Jiang, N., Ebert, P.J.R., Kidd, B.A., Muller, S. Lund, P.J., Juang, J., Adachi, K., Tse, T., Birnbaum, M.E., Newell, E.W., Wilson, D.M., Grotenbreg, G.M., Valitutti, S., Quake, S.R., and Davis, M.M. Clonal deletion prunes, but does not eliminate self-specific ab CD8+ T lymphocytes. Immunity, 42(5): 929-941, 2015.