Kevin Eislmayr

This study establishes a mouse model to investigate adaptive immunity to oral Shigella infection and identifies CD4+ T cells as critical for cross-serotype protection through IFN-gamma and IgA production.

This study identifies OspF as a Shigella effector that inhibits NAIP-NLRC4 inflammasome activation by blocking p38-dependent priming, explaining human susceptibility to Shigella.

This study identifies macrophages, not neutrophils, as key in controlling Shigella through TLR-induced IL-12 and IFN-γ in a mouse model of shigellosis.