Graduate Student

Department of Pathology
3-501 Bowen Science Building
51 Newton Road
University of Iowa
Iowa City, IA 52242

Lab: 319-384-2929


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


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 CD11alow/CD8ahigh CD8 or CD11alow/CD49dlow 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.