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• W2108961981 abstract "Abstract Mycobacterium tuberculosis is a virulent intracellular pathogen that survives in macrophages even in the presence of an intact adaptive immune response. Type I IFNs have been shown to exacerbate tuberculosis in mice and to be associated with disease progression in infected humans. Nevertheless, the mechanisms by which type I IFNs regulate the host response to M. tuberculosis infection are poorly understood. In this study, we show that M. tuberculosis induces an IFN-related gene expression signature in infected primary human macrophages, which is dependent on host type I IFN signaling as well as the mycobacterial virulence factor, region of difference-1. We further demonstrate that type I IFNs selectively limit the production of IL-1β, a critical mediator of immunity to M. tuberculosis. This regulation occurs at the level of IL1B mRNA expression, rather than caspase-1 activation or autocrine IL-1 amplification and appears to be preferentially used by virulent mycobacteria since avirulent M. bovis bacillus Calmette-Guérin (BCG) fails to trigger significant expression of type I IFNs or release of mature IL-1β protein. The latter property is associated with decreased caspase-1–dependent IL-1β maturation in the BCG-infected macrophages. Interestingly, human monocytes in contrast to macrophages produce comparable levels of IL-1β in response to either M. tuberculosis or BCG. Taken together, these findings demonstrate that virulent and avirulent mycobacteria employ distinct pathways for regulating IL-1β production in human macrophages and reveal that in the case of M. tuberculosis infection the induction of type I IFNs is a major mechanism used for this purpose." @default.
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• W2108961981 date "2011-09-01" @default.
• W2108961981 modified "2023-10-01" @default.
• W2108961981 title "<i>Mycobacterium tuberculosis</i> Triggers Host Type I IFN Signaling To Regulate IL-1β Production in Human Macrophages" @default.
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• W2108961981 doi "https://doi.org/10.4049/jimmunol.1100926" @default.
• W2108961981 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3159798" @default.
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• W2108961981 hasPublicationYear "2011" @default.
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