Emory Warner Research Fellow
robert-strother@uiowa.edu

Department of Pathology
3-500 Bowen Science Building
51 Newton Road
University of Iowa
Iowa City, IA 52242-1109

Lab: 319-384-2929

Training

Bachelor of Science Iowa State University

Research

Sepsis, a severe infection leading to organ dysfunction and possible death, is a major cause of mortality in the healthcare setting. Using the cecal ligation and puncture (CLP) model of sepsis-induction the Badovinac lab has demonstrated that sepsis compromises primary and secondary CD8 T cell responses to pathogen-derived antigens. Importantly, in some instances sepsis leads to long lasting impairement of CD8 T cell responses despite the numerical recovery of CD8 T cell compartment. The sepsis-induced mechanism(s) that control this impairment in CD8 T cells is currently unknown.

Dendritic Cells (DC) are antigen presenting cells (APC) that present antigen to T cells and are important for priming naïve CD8 T cells. Previous research has indicated that sepsis leads to a decrease in dendritic cell number and function. My project will use CLP model of sepsis induction to further investigate the extent to which sepsis influences the ability of DC to control CD8 T cell mediated immunity.

Publications

  1. Strother RK, DB Danahy, DI Kotov, TA Kucaba, ZR Zacharias, TS Griffith, KL Legge, and VP Badovinac.  Polymicrobial sepsis diminishes dendritic cell numbers and function directly contributing to impaired primary CD8 T cell responses in vivo. J Immunol 197: 4301-4311 (2016) [PubMed]