M. Suresh, DVM, MVSc, PhD

Pathobiological Sciences
3172 Vet Med
2015 Linden Dr
Madison, WI 53706
(608) 265-9791
Focus Groups: 
DVM, Veterinary College, Univ. Agri. Sci. Bangalore, India
PhD, University of Minnesota
Research Summary: 
Molecular and cellular basis of T cell memory; CD8+ T cell responses in chronic viral infections
Research Detail: 

Mechanisms of T-Cell Memory and Protective Immunity to Intracellular Pathogens Establishment and maintenance of protective memory B and T cells is fundamental to the development of effective vaccines. To date, protection afforded by the most effective vaccines depend upon the elicitation of neutralizing antibodies. However, protection against diseases such as Tuberculosis, Malaria and HIV would also require memory CD8 T cells. The overarching goal of our research therefore, is to understand the cellular and molecular basis of T cell memory to systemic and mucosal infections. In an immune response, naïve T cells differentiate into effector cells and a fraction of effector cells further differentiate into long-lived memory T cells. We are interested in identifying the signaling pathways and transcriptional mechanisms that regulate the differentiation and long-term persistence of systemic and tissue resident memory T cells. First, we are elucidating the metabolic and transcriptional basis for the programming of durable CD8 T-cell memory by the PI3K/AKT and NF-KB signaling pathways. Mechanistic information from these studies will pave the path for developing vaccination strategies to modulate signaling pathways in order to engender durable and protective CD8 T cell memory. Second, it is becoming increasingly clear that the combination and nature of innate immune signals play a vital role in programming protective T-cell memory. We are currently exploring the use of combination adjuvants that engage multiple innate immune pathways and engender potent and durable systemic and mucosal T-cell memory to non-replicating antigens.


Selected Publications: 
Sullivan, J. A., E.H. Kim, E. Plisch, and M. Suresh (2012) FOXO3 regulates the CD8 T cell response to a chronic viral infection. J. Virol. (Accepted).
Kim, E.H., J. S. Sullivan E. H. Plisch, M. M. Tejera, A. Jatzek, K. Y. Choi, and M. Suresh (2012) Signal integration by Akt regulates CD8 T cell effector and memory differentiation. J. Immunol. 188(9):4305-14. Epub 2012 Mar 30.
Sullivan, J. A., E. H. Kim, E. Plisch, S. L. Peng, and M. Suresh (2012) FOXO3 regulates CD8 T cell memory by T cell-intrinsic mechanisms. PLOS Pathog. 8(2):e1002533. Epub 2012 Feb 16.
Walsh, K., J. Teijaro, P. Wilker, A. Jatzek, D. Fremgen, S. Das, T. Watanabe, M. Hatta, K. Shinya, M. Suresh, Y. Kawaoka, H. Rosen, and M. Oldstone (2011) Suppression of cytokine storm with a sphingosine analog provides protection against pathogenic influenza virus. Proc. Natl. Acad. Sci. USA. 108(29):12018-12023.
Nanjappa, S. G., E. H. Kim, and M. Suresh (2011) Immunotherapeutic effects of IL-7 during a chronic viral infection in mice. Blood. 117(19): 5123-5132
Singh, A., A. Jatzek, E. H. Plisch, R. Srinivasan, J. Svaren, and M. Suresh (2010) Regulation of memory CD8 T cell differentiation by p27Kip1. Mol. Cell. Biol. 30(21):5145-59. PMC2953046
Nakayama, Y., E. H. Plisch, J. Sullivan, C. J. Czuprynski, B. R. J. Williams, and M. Suresh (2010) Role of PKR and Type I IFNs in viral control during primary and secondary infection. PLoS Pathog. 6(6):e1000966. PMC2891951
Hatta, Y, K. Hershberger, K. Shinya, S. C. Proll, R. R. Dubielzig, M. Hatta, M. G. Katze, Y. Kawaoka, and M. Suresh (2010) Viral replication rate regulates clinical outcome and CD8 T cell responses during highly pathogenic H5N1 virus infection. PLOS Pathog. 6(10): e1001139. PMC2951384.
Nakayama, Y., C. J. Czuprynski, B. R. J. Williams, and M. Suresh (2009). PKR ad type I IFNs are dispensable for memory T cell expansion but required for viral control during primary and secondary infections. J. Clin. Invest. (In review)
Singh, A., E. H. Plisch, and M. Suresh (2008) p27Kip1 constrains the quantity and quality of CD8 T cell memory by enforcing cell cycle exit of memory precursor effector cells. J. Exp. Med. (Submitted).