| pubmed-article:20436908 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C1335872 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:20436908 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:20436908 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:20436908 | pubmed:dateCreated | 2010-5-3 | lld:pubmed |
| pubmed-article:20436908 | pubmed:abstractText | Autocrine priming of cells by small quantities of constitutively produced type I interferon (IFN) is a well-known phenomenon. In the absence of type I IFN priming, cells display attenuated responses to other cytokines, such as anti-viral protection in response to IFNgamma. This phenomenon was proposed to be because IFNalpha/beta receptor1 (IFNAR1) is a component of the IFNgamma receptor (IFNGR), but our new data are more consistent with a previously proposed model indicating that regulated expression of STAT1 may also play a critical role in the priming process. Initially, we noticed that DNA binding activity of STAT1 was attenuated in c-Jun(-/-) fibroblasts because they expressed lower levels of STAT1 than wild-type cells. However, expression of STAT1 was rescued by culturing c-Jun(-/-) fibroblasts in media conditioned by wild-type fibroblasts suggesting they secreted a STAT1-inducing factor. The STAT1-inducing factor in fibroblast-conditioned media was IFNbeta, as it was inhibited by antibodies to IFNAR1, or when IFNbeta expression was knocked down in wild-type cells. IFNAR1(-/-) fibroblasts, which cannot respond to this priming, also expressed reduced levels of STAT1, which correlated with their poor responses to IFNgamma. The lack of priming in IFNAR1(-/-) fibroblasts was compensated by over-expression of STAT1, which rescued molecular responses to IFNgamma and restored the ability of IFNgamma to induce protective anti-viral immunity. This study provides a comprehensive description of the molecular events involved in priming by type I IFN. Adding to the previous working model that proposed an interaction between type I and II IFN receptors, our work and that of others demonstrates that type I IFN primes IFNgamma-mediated immune responses by regulating expression of STAT1. This may also explain how type I IFN can additionally prime cells to respond to a range of other cytokines that use STAT1 (e.g., IL-6, M-CSF, IL-10) and suggests a potential mechanism for the changing levels of STAT1 expression observed during viral infection. | lld:pubmed |
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| pubmed-article:20436908 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20436908 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20436908 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:20436908 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20436908 | pubmed:issn | 1545-7885 | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:LevyDavid EDE | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:SabapathyKana... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:JohnstoneRick... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:TrapaniJoseph... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:HertzogPaul... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:ClarkeChristo... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:GouldJodee... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:GoughDaniel... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:MessinaNicole... | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:HiiLindaL | lld:pubmed |
| pubmed-article:20436908 | pubmed:author | pubmed-author:RobertsonAshl... | lld:pubmed |
| pubmed-article:20436908 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20436908 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:20436908 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20436908 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20436908 | pubmed:pagination | e1000361 | lld:pubmed |
| pubmed-article:20436908 | pubmed:dateRevised | 2010-9-30 | lld:pubmed |
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| pubmed-article:20436908 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20436908 | pubmed:articleTitle | Functional crosstalk between type I and II interferon through the regulated expression of STAT1. | lld:pubmed |
| pubmed-article:20436908 | pubmed:affiliation | Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia. | lld:pubmed |
| pubmed-article:20436908 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20436908 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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