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NAD + Depletion Triggers Macrophage Necroptosis, a Cell Death Pathway Exploited by Mycobacterium tuberculosis

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Ferritin H Deficiency in Myeloid Compartments Dysregulates Host Energy Metabolism and Increases Susceptibility to Mycobacterium tuberculosis Infection

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Is Receptor-Interacting Protein Kinase 3 a Viable Therapeutic Target for Mycobacterium tuberculosis Infection?

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Autophagy promotes ferroptosis by degradation of ferritin

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Pharmacological Inhibition of Host Heme Oxygenase-1 Suppresses Mycobacterium tuberculosis Infection In Vivo by a Mechanism Dependent on T Lymphocytes

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A Novel Antimycobacterial Compound Acts as an Intracellular Iron Chelator

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Ferrostatins Inhibit Oxidative Lipid Damage and Cell Death in Diverse Disease Models

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Mycobacterium tuberculosis acquires iron by cell-surface sequestration and internalization of human holo-transferrin

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Mycobacterium tuberculosis is extraordinarily sensitive to killing by a vitamin C-induced Fenton reaction

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Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death

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Efferocytosis Is an Innate Antibacterial Mechanism

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Autophagy protects against active tuberculosis by suppressing bacterial burden and inflammation

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Innate and Adaptive Interferons Suppress IL-1α and IL-1β Production by Distinct Pulmonary Myeloid Subsets during Mycobacterium tuberculosis Infection

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Mycobacterium tuberculosis Induces an Atypical Cell Death Mode to Escape from Infected Macrophages

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Human Macrophages Infected with a High Burden of ESAT-6-Expressing M. tuberculosis Undergo Caspase-1- and Cathepsin B-Independent Necrosis

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Mycobacterium tuberculosis evades macrophage defenses by inhibiting plasma membrane repair

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Mycobacterium tuberculosis Senses Host-Derived Carbon Monoxide during Macrophage Infection

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