| pubmed-article:21622562 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:21622562 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
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| pubmed-article:21622562 | lifeskim:mentions | umls-concept:C2003905 | lld:lifeskim |
| pubmed-article:21622562 | pubmed:issue | 30 | lld:pubmed |
| pubmed-article:21622562 | pubmed:dateCreated | 2011-7-25 | lld:pubmed |
| pubmed-article:21622562 | pubmed:abstractText | Protection against infection with Mycobacterium tuberculosis demands IFN-?. SOCS1 has been shown to inhibit responses to IFN-? and might thereby play a central role in the outcome of infection. We found that M. tuberculosis is a highly efficient stimulator of SOCS1 expression in murine and human macrophages and in tissues from infected mice. Surprisingly, SOCS1 reduced responses to IL-12, resulting in an impaired IFN-? secretion by macrophages that in turn accounted for a deteriorated intracellular mycobacterial control. Despite SOCS1 expression, mycobacteria-infected macrophages responded to exogenously added IFN-?. SOCS1 attenuated the expression of the majority of genes modulated by M. tuberculosis infection of macrophages. Using a conditional knockdown strategy in mice, we found that SOCS1 expression by macrophages hampered M. tuberculosis clearance early after infection in vivo in an IFN-?-dependent manner. On the other hand, at later time points, SOCS1 expression by non-macrophage cells protected the host from infection-induced detrimental inflammation. | lld:pubmed |
| pubmed-article:21622562 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:21622562 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:21622562 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21622562 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:21622562 | pubmed:issn | 1083-351X | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:WigzellHansH | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:YoshimuraAkih... | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:SinghMahavirM | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:Gavier-WidénD... | lld:pubmed |
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| pubmed-article:21622562 | pubmed:author | pubmed-author:SköldMarkusM | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:OehlmannWulfW | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:BhujuSabinS | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:CarowBeritB | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:YeXiang qunX | lld:pubmed |
| pubmed-article:21622562 | pubmed:author | pubmed-author:IgnatowiczLec... | lld:pubmed |
| pubmed-article:21622562 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21622562 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:21622562 | pubmed:volume | 286 | lld:pubmed |
| pubmed-article:21622562 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21622562 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21622562 | pubmed:pagination | 26873-87 | lld:pubmed |
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| pubmed-article:21622562 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21622562 | pubmed:articleTitle | Silencing suppressor of cytokine signaling-1 (SOCS1) in macrophages improves Mycobacterium tuberculosis control in an interferon-gamma (IFN-gamma)-dependent manner. | lld:pubmed |
| pubmed-article:21622562 | pubmed:affiliation | Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm 17177, Sweden. | lld:pubmed |
| pubmed-article:21622562 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21622562 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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