Igor Kramnik

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

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 paper introduces a protocol for 3D multiplexed immunohistochemistry using Opal-TSA conjugated fluorescent dyes to enhance imaging of pulmonary TB lesions in mouse tissues.

This study identifies new genetic loci and candidate genes associated with tuberculosis susceptibility in mice using systems genetics approaches.

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.