Vladimir Badovinac Laboratory—Department of Pathology

  • Stephanie A. Condotta, PhD

    Stephanie Condotta, Postdoctoral Research Scholar

    Postdoctoral Research Fellow
     stephanie-condotta@uiowa.edu

    Department of Pathology
    1160 Medical Laboratories
    500 Newton Road
    University of Iowa
    Iowa City, IA 52242-1109

    Lab: 319-384-2929

    Training

    PhD, Microbiology and Immunology, The University of British Columbia, 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.

    Fellowship

    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.

    Publications

    1. 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 2013: 33(1): 23-40.
    2. 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. 2013; 190(5): 1991-2000.
    3. Condotta SA, Richer MJ, Badovinac VP, Harty JT. Probing CD8 T cell responses with Listeria monocytogenes infection. Adv Immunol. 2012; 113: 51-80.
    4. 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. 2012; 188(3): 1255-65.
    5. 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. 2011; 187(5): 2148-54.
    6. Martin MM, Condotta SA, Fenn J, Olmstead AD, Jean F. In-cell selectivity profiling of membrane-anchored and replicase-associated hepatitis C virus NS3-4A protease reveals a common stringent substrate recognition profile. Biol Chem. 2011; 392(10): 927-35.
    7. Condotta SA, Martin MM, Boutin M, Jean F. Detection and in-cell selectivity profiling of the full-length West Nile virus NS2B/NS3 serine protease using membrane-anchored fluorescent substrates. Biol Chem. 2010; 391(5): 549-59. Cover illustration.
    8. Condotta SA, Hunter FF, Bidochka MJ. West Nile Virus Infection Rates in Pooled and Individual Mosquito Samples. Vector Borne Zoonotic Dis. 2004; 4(3):198-203.