Our main (and everchanging) research goals with non-exhaustive list of papers published are:

Research Diagram 1, see text

Naive, effector, and memory T cells generated after acute infection/vaccination. Naïve T cells exist at low numbers with minimal functionality and protective capacity but vigorously proliferate upon cognate Ag-stimulation, generating a sizable effector pool with ample functionality and protective capacity but have a diminished life span. The effector T cells that survive the contraction phase will form a heterogeneous population of long-lived memory

CD8 T cells and maintain their effector function and protective capability.

Diagram, read the text for a full description

Memory CD8 T cell phenotype and function is dependent on the history of Ag-encounters.Functional characteristics of memory CD8 T cells that have encountered Ag multiple (1-4) times. Functional abilities and characteristics are highest for memory populations at the outermost edges and progressively decrease for memory populations moving inward (i.e. proliferative expansion 1°>2°>3°>4°)

Research Diagram, see text

Pathogen-specific CD8 T cells can be identified using 'surrogate activation markers' approach.

After infection, pathogen-specific CD8 T cells upregulate the surface expression of the integrin CD11a and downregulate surface expression of CD8a, while surface expression of these molecules remains unchanged in naïve Ag-inexperienced CD8 T cells.

These surface phenotype changes can help distinguish pathogen-specific from naïve CD8 T cells after infection without knowledge of specific antigenic epitopes or host MHC restriction elements.

Research Diagram, see text

Sepsis diminishes localized CD8 T cell-mediated immunity. In a healthy host, tissue resident memory CD8 T cells (TRM) and circulating memory (TCIRCM) CD8

Tand B cells are evoked upon infection (A) and re-infection induces TRM production of IFN-γ, endothelial cell upregulation of chemokines and adhesion molecules, influx of memory T and B cells from the circulation and pathogen clearance (C). Sepsis induces a dramatic numerical loss of TCIRCM but not TRM (B), endothelial cells are unable to respond to the IN-γ signal, few effector cells are recruited from the circulation and pathogen clearance is significantly impaired (D).