I. Kramnik

Lipid Peroxidation and Type I Interferon Coupling Fuels Pathogenic Macrophage Activation Causing Tuberculosis Susceptibility

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

Aberrant macrophage activation and maladaptive lung repair promote tuberculosis progression uniquely in the lung

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

Perivascular and peribronchiolar granuloma-associated lymphoid tissue and B-cell gene expression pathways identify asymptomatic Mycobacterium tuberculosis lung infection in Diversity Outbred mice{-}{-}{-}

The paper identifies B-cell gene expression pathways and imaging biomarkers associated with asymptomatic Mycobacterium tuberculosis infection in mice.

Cell state transition analysis identifies interventions that improve control of M. tuberculosis infection by susceptible macrophages

The paper identifies chemical perturbations that shift the transcriptional state of TB-susceptible macrophages toward TB-resistant cells, improving resistance to M. tuberculosis.

Adjunctive inhibition of the integrated stress response pathway accelerates bacterial clearance in a mouse model of tuberculosis

This study shows that inhibiting the Integrated Stress Response (ISR) pathway alongside standard TB antibiotics reduces bacterial loads and accelerates sterilization in a mouse model of tuberculosis.

Dissemination and progression of pulmonary Mycobacterium avium infection in mouse model are associated with type 2 macrophage activation

This study shows that B6.Sst1S mice develop more severe pulmonary M. avium infection with increased type 2 macrophage activation and reduced T cell density compared to wild-type mice.

Maladaptive oxidative stress cascade drives type I interferon hyperactivity in TNF activated macrophages promoting necrosis in murine tuberculosis granulomas

This study identifies a maladaptive oxidative stress cascade in TNF-activated macrophages that drives IFN-I hyperactivity and necrosis in murine tuberculosis granulomas, with potential therapeutic targets identified.

Channeling macrophage polarization via selective translation inhibition by rocaglates increases macrophage resistance to Mycobacterium tuberculosis

This study shows rocaglates shift macrophage polarization toward M1-like by inhibiting IL-4 response and enhancing resistance to Mycobacterium tuberculosis.

Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons

This study identifies SP140 as a repressor of type I interferons that enhances resistance to bacterial infections like Legionella pneumophila and Mycobacterium tuberculosis.

Spatial and temporal localization of immune transcripts defines hallmarks and diversity in the tuberculosis granuloma

The paper uses in situ sequencing to analyze immune transcript localization in tuberculosis granulomas, revealing time-dependent immune landscape changes and spatial transcriptomic patterns.

The integrated stress response mediates type I interferon driven necrosis in Mycobacterium tuberculosis granulomas

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.