Kurt Schesser

Murine neonates are highly resistant to Yersinia enterocolitica following orogastric exposure.

The activities of the Yersinia protein kinase A (YpkA) and outer protein J (YopJ) virulence factors converge on an eIF2alpha kinase.

Yersinia enterocolitica promotes robust mucosal inflammatory T-cell immunity in murine neonates.

The outer membrane protein A (OmpA) of Yersinia pestis promotes intracellular survival and virulence in mice.

Host innate recognition of an intestinal bacterial pathogen induces TRIF-dependent protective immunity.

Eukaryotic initiation factor 2 (eIF2) signaling regulates proinflammatory cytokine expression and bacterial invasion.

The host-encoded Heme Regulated Inhibitor (HRI) facilitates virulence-associated activities of bacterial pathogens.

The Yersinia pestis type III secretion system: expression, assembly and role in the evasion of host defenses.

Murine neonates infected with Yersinia enterocolitica develop rapid and robust proinflammatory responses in intestinal lymphoid tissues.

Pathogenic Yersinia Promotes Its Survival by Creating an Acidic Fluid-Accessible Compartment on the Macrophage Surface.

TIR Domain-Containing Adapter-Inducing Beta Interferon (TRIF) Mediates Immunological Memory against Bacterial Pathogens.

Perforin-2 Protects Host Cells and Mice by Restricting the Vacuole to Cytosol Transitioning of a Bacterial Pathogen.

The eIF2α Kinase Heme-Regulated Inhibitor Protects the Host from Infection by Regulating Intracellular Pathogen Trafficking.