Russell E. Vance

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.

The paper shows that sustained type I IFN signaling in infected macrophages impairs IFNγ responses, leading to tuberculosis susceptibility.

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 shows that Mycobacterium tuberculosis is resistant to innate immune clearance even under conditions that enhance innate immunity.

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.

This study identifies SP140's role in regulating IFN-β mRNA stability through RESIST, revealing a dual antiviral and interferon regulatory function.

The paper identifies a poxvirus effector that triggers an NF-κB response by disrupting anti-viral complexes, revealing a novel ETI pathway.

This paper identifies proteolytic cleavage as the mechanism regulating fungal gasdermin activity, showing that HET-Q1 is cleaved by HET-Q2 to induce cell death and that gasdermin genes are clustered with protease genes.

The paper shows that defective microglial pyroptosis in mice leads to ADHD-like behaviors, suggesting a link between microglial cell death and neurodevelopmental disorders.

This study identifies IL-1Ra as a mediator of type I IFN-driven susceptibility to Mtb in a mouse model, showing that reducing IL-1Ra levels protects against infection.