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Nitric Oxide Modulates Macrophage Responses toMycobacterium tuberculosisInfection through Activation of HIF-1α and Repression of NF-κB

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HIF-1α Is an Essential Mediator of IFN-γ–Dependent Immunity toMycobacterium tuberculosis

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Interleukin 27R regulates CD4+T cell phenotype and impacts protective immunity duringMycobacterium tuberculosisinfection

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Hypoxia Inducible Factor Signaling Modulates Susceptibility to Mycobacterial Infection via a Nitric Oxide Dependent Mechanism

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