Lester Kobzik

This study identifies aberrant macrophage activation and maladaptive lung repair as key factors promoting tuberculosis progression in the lung using a novel mouse model.

This paper describes a mouse model of post-primary pulmonary tuberculosis that simulates hematogenous spread to the lungs and allows study of lung-specific TB mechanisms.

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 identifies the integrated stress response (ISR) as a mediator of necrosis in tuberculosis granulomas, showing that ISR inhibition reduces bacterial burden and necrosis in susceptible mice.

The paper identifies a dysregulated macrophage response to TNF in sst1-deficient mice, leading to increased susceptibility to intracellular bacteria and necrotic inflammation.