Stephanie A. Condotta, PhD

Research Associate 2010-2014


Postdoctoral Research Fellow, University of Iowa 2010-2014
PhD, The University of British Columbia, Microbiology and Immunology, Vancouver, BC, Canada, 2005-2010
MS, Brock University, Centre for Biotechnology, St. Catharines, ON, Canada, 2002-2005
BS, Brock University, Centre for Biotechnology, St. Catharines, ON, Canada, 1997-2002

Research Interests

Sepsis is a major public heath problem that can affect anyone at anytime. Patients that survive severe sepsis often display compromised innate and adaptive immunity. This immunosuppressive state is exhibited by susceptibility to ‘secondary’ infections with intracellular pathogens that are normally controlled by CD8 T cells. CD8 T cells play an important role in the control and elimination of intracellular pathogens. Thus, alterations in the naïve CD8 T cell repertoire can seriously compromise T cell immunity. Little is known about the long-term immune consequences for an individual that has survived sepsis. My current research focuses on understanding the long-term consequences of sepsis on CD8 T cell homeostasis and if this impacts the ability of CD8 T cells to respond to pathogenic challenge.


American Heart Association, Midwest Affiliate, Winter 2013 Postdoctoral Fellowship. Sepsis induced changes in naïve and memory CD8 T cell responses to newly encountered infections. Duration: July 1, 2013 to June 30, 2015.


  1. Sjaastad FV, SA Condotta, JA Kotov, KA Pape, C Dail, DB Danahy, TA Kucaba, LT Tygrett, KA Murphy, J Cabrera-Perez, TJ Waldschmidt, VP Badovinac, TS Griffith. Polymicrobial Sepsis Chronic Immunoparalysis Is Defined by Diminished Ag-Specific T Cell-Dependent B Cell Responses. Front Immunol 9:2532 (2018) [PubMed]
  2. Condotta SA, Khan SH, Rai D, Griffith TS, Badovinac VP. Polymicrobial sepsis increases susceptibility to chronic viral infection and exacerbates CD8+ T cell exhaustion. J Immunol 195: 116-125 (2015).
  3. Cabrera-Perez J, Condotta SA, James BR, Kashem SW, Brincks EL, Rai D, Kucaba TA, Badovinac VP, Griffith TS. Alterations in antigen-specific naïve CD4 T cell precursors after sepsis impairs their responsiveness to pathogen challenge. J Immunol 194: 1609-1620 (2015).
  4. Markwart R, Condotta SA, Requardt RP, Borken F, Schubert K, Weigel C, Bauer M, Griffith TS, Förster M, Brunkhorst FM, Badovinac VP, Rubio I. Immunosuppression after sepsis: systemic inflammation and sepsis induce a loss of naïve T-cells but no enduring cell-autonomous defects in T-cell function. PLoS One 9: e115094 (2014).
  5. Cabrera-Perez J, Condotta SA, Badovinac VP and Griffith TS. Impact of sepsis on CD4 T cell immunity. J Leukoc Biol 96: 767-777 (2014).
  6. Duong S, Condotta SA, Rai D, Martin MD, Griffith TS and Badovinac VP. Polymicrobial sepsis alters antigen-dependent and -independent memory CD8 T cell functions. J Immunol 192: 3618-3625 (2014).
  7. Condotta, SA, J Cabrera-Perez, VP Badovinac and TS Griffith. T-cell mediated immunity and the role of TRAIL in sepsis-induced immunosuppression. Crit Rev Immunol 33: 23-40 (2013).
  8. Condotta SA, Rai D, James BR, Griffith TS, Badovinac VP. Sustained and Incomplete Recovery of Naive CD8+ T Cell Precursors after Sepsis Contributes to Impaired CD8+ T Cell Responses to Infection. J Immunol 190: 1991-2000 (2013).
  9. Condotta SA, Richer MJ, Badovinac VP, Harty JT. Probing CD8 T cell responses with Listeria monocytogenes infection. Adv Immunol 113: 51-80 (2012).
  10. Martin MD, Condotta SA, Harty JT, Badovinac VP. Population dynamics of naïve and memory CD8 T cell responses after antigen stimulations in vivo. J Immunol 188: 1255-1265 (2012).
  11. Gurung P, Rai D, Condotta SA, Babcock JC, Badovinac VP, Griffith TS. Immune unresponsiveness to secondary heterologous bacterial infection after sepsis induction is TRAIL dependent. J Immunol 187: 2148-2154 (2011).
Stephanie Condotta