Sarah E.F. D'Orazio

The Listeria monocytogenes lemA gene product is not required for intracellular infection or to activate fMIGWII-specific T cells.

H2-M3-restricted CD8+ T cells are not required for MHC class Ib-restricted immunity against Listeria monocytogenes.

Cytosolic localization of Listeria monocytogenes triggers an early IFN-gamma response by CD8+ T cells that correlates with innate resistance to infection.

Use of the CD107 mobilization assay reveals that cytotoxic T lymphocytes with novel MHC-Ib restriction are activated during Listeria monocytogenes infection.

Multiple mechanisms contribute to the robust rapid gamma interferon response by CD8+ T cells during Listeria monocytogenes infection.

Lymphocytes serve as a reservoir for Listeria monocytogenes growth during infection of mice.

Heat shock factor 1 protects mice from rapid death during Listeria monocytogenes infection by regulating expression of tumor necrosis factor alpha during fever.

T cell-intrinsic factors contribute to the differential ability of CD8+ T cells to rapidly secrete IFN-γ in the absence of antigen.

Human CD8+ T cells display a differential ability to undergo cytokine-driven bystander activation.

InlA promotes dissemination of Listeria monocytogenes to the mesenteric lymph nodes during food borne infection of mice.