PhD, Interdisciplinary Graduate Program in Immunology, University of Iowa, 2019
Bachelor of Science in Microbiology - University of Kansas
Sepsis is characterized by a systemic infection resulting in organ failure. Sepsis related complications currently account for 33-50% of all hospital deaths. Patients that survive a septic event are more susceptible to infection. The Badovinac lab focuses on CD8 T cells which provide protection against viral and bacterial infections. Our lab has shown that sepsis leads to cell death of both naïve and memory CD8 T cells resulting in increased susceptibility to new, or previously encountered infections.
Tissue-resident memory (TRM) is a recently discovered CD8 T cell subset. These cells survey barrier tissues that are commonly exploited by pathogens to enter the host and cause infection. During a localized infection, TRM rapidly provide protection by recruiting and activating immune cells at the site of pathogen entry. It is not currently known the extent to which sepsis affects TRM. I will start addressing this by elucidating the impact of sepsis on TRM numbers, metabolism and protective capacity.
Publications associated with the lab
- Moioffer SJ*, DB Danahy*, S van de Wall, IJ Jensen, FV Sjaastad, SM Anthony, JT Harty, TS Griffith, and VP Badovinac. Severity of sepsis determines the degree of impairment observed in circulatory and tissue-resident memory CD8 T cell populations. J Immunol 207: 1871-1881 (2021) [PubMed]
- Shan Q, S Hu, X Chen, DB Danahy, VP Badovinac, C Zhang, and HH Xue. Ectopic Tcf1 expression instills a stem-like program in exhausted CD8 T cells to enhance viral and tumor immunity. Cell Mol Immunol 18: 1262-1277 (2021) [PubMed]
- Danahy DB, RB Berton, and VP Badovinac. Cutting Edge: Anti-tumor immunity by pathogen-specific CD8 T cells in the absence of cognate antigen recognition. J Immunol 204: 1431-1435 (2020) [PubMed]
- Danahy DB, SP Kurup, CS Winborn, IJ Jensen, JT Harty, TS Griffith, VP Badovinac. Sepsis-Induced State of Immunoparalysis Is Defined by Diminished CD8 T Cell-Mediated Antitumor Immunity. J Immunol 203: 725-735 (2019) [PubMed]
- Huggins MA, FV Sjaastad, M Pierson, TA Kucaba, W Swanson, C Staley, AR Weingarden, IJ Jensen, DB Danahy, VP Badovinac, SC Jameson, V Vezys, D Masopust, A Khortus, TS Griffith, and SE Hamilton. Microbial exposure enhances immunity to pathogens recognized by TLR2 but increases susceptibility to cytokine storm via TLR4 sensitization. Cell Rep 28: 1729-1743 (2019) [PubMed]
- Danahy DB, IJ Jensen, TS Griffith, VP Badovinac. Cutting Edge: Polymicrobial Sepsis Has the Capacity to Reinvigorate Tumor-Infiltrating CD8 T Cells and Prolong Host Survival. J Immunol 202: 2843 (2019) [PubMed]
- 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]
- Martin MD, DB Danahy, SM Hartwig, JT Harty, and VP Badovinac. Revealing the Complexity in CD8 T Cell Responses to Infection in Inbred C57B/6 versus Outbred Swiss Mice. Front Immunol 8:1527 (2017) [PubMed]
- Danahy DB, SM Anthony, IJ Jensen, SM Hartwig, Q Shan, HH Xue, JT Harty, TS Griffith, and VP Badovinac. Polymicrobial sepsis impairs bystander recruitment of effector cells to infected skin despite optimal sensing and alarming function of skin resident memory CD8 T cells. PLoS Pathog 13: 9 (2017) [PubMed]
- 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]
- Danahy DB, RK Strother, VP Badovinac, and TS Griffith. Clinical and experimental sepsis impair T cell-mediated immunity. Crit Rev Immunol 36: 57-74 (2016) [PubMed]