Education

Bachelor of Science in Biology- California State University, Stanislaus
Master of Science in Biology- California State University, Los Angeles

Research

I am interested in examining how sepsis induces alterations of the Naïve CD8 T Cell Compartment. Sepsis is characterized by a disseminated infection, resulting in a hyperinflammatory state, followed by prolonged immunoparalysis which is characterized by severe transient lymphopenia and long-lasting immunological dysregulation.

Our lab focus on naïve and memory CD8 T cell responses after acute infections and/or vaccinations. Upon cognate antigen-encounter naïve Ag-specific CD8 T cells undergo proliferative expansion in numbers and differentiate into effector cells that contribute to pathogen clearance.  Thus, the status of naïve CD8 T cell compartment can determine the ability of the host to respond to newly encountered infections.

Sepsis induces rapid and vigorous apoptosis of naïve (Ag-non experienced CD11a^low/CD8a^high CD8 or CD11a^low/CD49d^low CD4 T cells) T cells creating a lymphopenic environment supporting homeostatic proliferation (HP) of T cells that survive early ‘cytokine storm’ phase of sepsis. As a consequence of HP and in response to microbes that evoke sepsis, numerical recovery of T cell compartment is accompanied by phenotypic/functional changes (memory-like T cells) on a sizeable fraction of T cells. Sepsis can induce ‘holes’ in the T cell repertoire further contributing to overall changes in the composition of T cell pools, making their subsequent T cell responses to newly encountered pathogens potentially impaired.

One of my projects will be to further delineate sepsis-induced long-lasting functional, epigenetic, and transcriptomic changes in naïve CD8 T cells using state-of-the-art techniques and models readily available in the lab.

Publications associated with the lab

1. Silva EE, SJ Moioffer, M Hassert, RR Berton, MG Smith, S Van de Wall, DK Meyerholz, TS Griffith, JT Harty, and VP Badovinac. Defining parameters that modulate susceptibility and protection to respiratory murine coronavirus MHV1 infection. J Immunol in press (2024)
2. Berton RR, PW McGonagill, IJ Jensen, TK Ybarra, GA Bishop, JT Harty, TS Griffith, and VP Badovinac. Sepsis leads to lasting changes in phenotype and function of naïve CD8 T cells. PLoS Pathog 10: e1011720 (2023) [PubMed]
3. Moioffer SJ, RR Berton, PW McGonagill, IJ Jensen, TS Griffith, and VP Badovinac. Inefficient recovery of repeatedly stimulated memory CD8 T cells after polymicrobial sepsis induction leads to changes in memory CD8 T cell pool composition. J Immunol 210: 168-179 (2023) [PubMed]
4. Berton RR, IJ Jensen, JT Harty, TS Griffith, and VP Badovinac. Inflammation controls susceptibility of immune experienced mice to sepsis. Immunohorizons 6: 825-842 (2022)[PubMed]
5. Jensen IJ, PW McGonagill, RR Berton, BA Wagner, EE Silva, GR Buettner, TS Griffith, and VP Badovinac. Prolonged ROS production following septic insult. Immunohorizons 5: 477-488 (2021) [PubMed]
6. Sjaastad FV, IJ Jensen, RR Berton, VP Badovinac, and TS Griffith.  Inducing experimental polymicrobial sepsis by cecal ligation and puncture.  Curr Protoc Immunol 131: e110 (2020) [PubMed]
7. Danahy DB, RR 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]