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Multiple Defects of Immune Cell Function in Mice with Disrupted Interferon-γ Genes

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Altered responses to bacterial infection and endotoxic shock in mice lacking inducible nitric oxide synthase

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Lack of Acidification inMycobacteriumPhagosomes Produced by Exclusion of the Vesicular Proton-ATPase

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Identification of nitric oxide synthase as a protective locus against tuberculosis

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Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages.

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Tuberculosis: Pathogenesis, Protection and Control

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Mouse model of X–linked chronic granulomatous disease, an inherited defect in phagocyte superoxide production

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Major histocompatibility complex class I-restricted T cells are required for resistance to Mycobacterium tuberculosis infection.

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Lipoarabinomannan, a possible virulence factor involved in persistence of Mycobacterium tuberculosis within macrophages

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Absence of Respiratory Burst in X-linked Chronic Granulomatous Disease Mice Leads to Abnormalities in Both Host Defense and Inflammatory Response to Aspergillus fumigatus

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Mice that lack the interferon-gamma receptor have profoundly altered responses to infection with Bacillus Calmette-Guérin and subsequent challenge with lipopolysaccharide.

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Interferon-gamma-treated murine macrophages inhibit growth of tubercle bacilli via the generation of reactive nitrogen intermediates

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Mycobacterium tuberculosis Is Strikingly More Virulent for Mice When Given via the Respiratory than via the Intravenous Route

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