M. B. Goldberg

This study identifies distinct neutrophil phenotypes linked to disease severity in hospitalized COVID-19 patients using longitudinal data and multi-omics analyses.

The paper identifies NLRP11 as a cytosolic receptor for bacterial lipopolysaccharide in human macrophages, essential for caspase-4 inflammasome activation.

The paper maps the topology of IpaB in Shigella translocons and shows its role in forming the pore channel for virulence protein delivery.

This paper identifies OspB as a cysteine protease in Shigella spp. and shows it interacts with the TORC1 pathway in yeast through proteolytic cleavage of Tco89p.

This study shows actin polymerization is required for T3SS translocon pore opening, enabling effector translocation, but not for docking or membrane insertion.

The paper profiles early humoral immune responses in COVID-19 patients, finding that survivors show rapid SARS-CoV-2-specific immunity linked to pre-existing OC43 immunity, while non-survivors have delayed and blunted responses.

The paper identifies a regulatory myeloid program, MS1, associated with sepsis mortality and up-regulated in severe COVID-19, showing its immunosuppressive role and cytokine-dependent induction.

This study shows that Shigella flexneri uses IpaC to reduce cell-cell tension, enabling intercellular spread by forming protrusions.

This paper shows that host intermediate filaments induce conformational changes in the Shigella T3SS pore, enabling docking and effector secretion.

The paper determines the topology of IpaC and SipC translocon pore proteins in their native context during infection, resolving conflicting data and identifying topological differences that may underlie functional divergence.