William R. Bishai

This study identifies intrinsic T-cell programming and pulmonary immune spatial organization as sex-dependent mechanisms governing tuberculosis immunity in mice.

This study identifies how IFN and mimetics prevent TB susceptibility by modulating iron metabolism and lipid peroxidation in macrophages.

This study shows that gonadal sex, not chromosomal sex, influences TB susceptibility in mice, with males showing myeloid dysfunction and females showing enhanced immune responses.

BCG therapy reduces tau pathology and improves cognitive function in PS19 mice by modulating myeloid cell activity and neuroinflammation.

This study shows that inhibiting glutamine metabolism with JHU083 enhances macrophage phagocytosis of Mtb by altering lipid metabolism and inflammatory markers.

This study shows that deleting the ESX-5 secretion system in Mycobacterium tuberculosis reduces ESX-5 substrate secretion, increases ESX-1 substrates, decreases ESX-3 expression, and alters cell morphology and antibiotic susceptibility.

This study evaluates a modified BCG vaccine overexpressing cyclic di-AMP, showing improved protection against TB in rhesus macaques.

This study shows that loss of the PPE71-38 locus in Mycobacterium tuberculosis Lineage 2 increases stress response gene expression and triglyceride levels, contributing to hypervirulence.

This paper presents a T-cell vaccine targeting conserved regions across Sarbecoviruses to provide cross-protection against evolving variants.

This study shows that APOE genotype affects neurovascular vulnerability in human forebrain organoids under viral stress, with APOE2/2 and APOE4/4 showing distinct inflammatory and vascular responses.

This study shows that senolytic drugs reduce tuberculosis progression in mice by eliminating senescent lung myeloid cells that promote disease.

This study identifies Myc dysregulation in macrophages as a driver of TB susceptibility by linking lipid peroxidation and IFN-I pathway hyperactivity.

This study corrects GBA mutations in hiPSCs to restore macrophage function in Gaucher disease and shows increased susceptibility to Mycobacterium tuberculosis.

This paper describes a second-generation diphtheria toxin-based fusion protein with reduced vascular leak and improved therapeutic activity in melanoma when used alone or with anti-PD-1.