| pubmed-article:21784976 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0026926 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C1167395 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:21784976 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:21784976 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:21784976 | pubmed:dateCreated | 2011-8-22 | lld:pubmed |
| pubmed-article:21784976 | pubmed:abstractText | 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-1?, 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-1? protein. The latter property is associated with decreased caspase-1-dependent IL-1? maturation in the BCG-infected macrophages. Interestingly, human monocytes in contrast to macrophages produce comparable levels of IL-1? in response to either M. tuberculosis or BCG. Taken together, these findings demonstrate that virulent and avirulent mycobacteria employ distinct pathways for regulating IL-1? 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. | lld:pubmed |
| pubmed-article:21784976 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21784976 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21784976 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21784976 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:21784976 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21784976 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21784976 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21784976 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:21784976 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:TrinchieriGio... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:FengCarl GCG | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:RabinRonald... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:SherAlanA | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:MyersTimothy... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:ThompsonRober... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:CardoneMarcoM | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:ShenderovKevi... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:NovikovAlekse... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:Mayer-BarberK... | lld:pubmed |
| pubmed-article:21784976 | pubmed:author | pubmed-author:KirschmanKevi... | lld:pubmed |
| pubmed-article:21784976 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21784976 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:21784976 | pubmed:volume | 187 | lld:pubmed |
| pubmed-article:21784976 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21784976 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21784976 | pubmed:pagination | 2540-7 | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:meshHeading | pubmed-meshheading:21784976... | lld:pubmed |
| pubmed-article:21784976 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21784976 | pubmed:articleTitle | Mycobacterium tuberculosis triggers host type I IFN signaling to regulate IL-1? production in human macrophages. | lld:pubmed |
| pubmed-article:21784976 | pubmed:affiliation | Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. | lld:pubmed |
| pubmed-article:21784976 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21784976 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:21784976 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
| entrez-gene:3553 | entrezgene:pubmed | pubmed-article:21784976 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21784976 | lld:entrezgene |
