pubmed-article:20626297 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0014038 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0025919 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0006104 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0151317 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0040557 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C1332821 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C1332691 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C1367714 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0332325 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:20626297 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:20626297 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:20626297 | pubmed:dateCreated | 2010-9-14 | lld:pubmed |
pubmed-article:20626297 | pubmed:abstractText | We examined the role of interferon-? (IFN-?) in expression of chemokine mRNA and proteins in the brain during chronic infection with Toxoplasma gondii using BALB/c and BALB/c-background IFN-? knockout (IFN-?(-/-)) mice. BALB/c mice are genetically resistant to development of toxoplasmic encephalitis and establish a latent, chronic infection in the brain through IFN-?-mediated immune responses. Amounts of mRNA for CXCL9/MIG, CXCL10/IP-10, CXCL11/I-TAC, CCL2/MCP-1, CCL3/MIP-1?, and CCL5/RANTES significantly increased in the brains of wild-type mice after infection. CXCL9/MIG, CXCL10/IP-10, and CCL5/RANTES mRNA were most abundant among these chemokines. An increase in amounts of mRNA for CXCL10/IP-10, CCL2/MCP-1, CCL3/MIP-1?, and CCL5/RANTES was also observed in the brains of IFN-?(-/-) mice after infection, although CXCL10/I-10 and CCL5/RANTES mRNA levels in infected IFN-?(-/-) mice were significantly lower than those of infected wild-type animals. Amounts of mRNA for CXCL9/MIG and CXCL11/I-TAC remained at the basal levels in infected IFN-?(-/-) mice. When amounts of the chemokine proteins were examined in the brain homogenates of uninfected and infected mice of both strains, large amounts of CXCL9/MIG, CXCL10/IP-10, and CCL5/RANTES were detected only in infected wild-type animals. These results indicate that CXCL9/MIG, CXCL10/IP-10, and CCL5/RANTES are the chemokines predominantly induced in the brains of genetically resistant BALB/c mice during chronic infection with T. gondii, and their expression is dependent on IFN-?. | lld:pubmed |
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pubmed-article:20626297 | pubmed:language | eng | lld:pubmed |
pubmed-article:20626297 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20626297 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20626297 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:20626297 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20626297 | pubmed:month | Sep | lld:pubmed |
pubmed-article:20626297 | pubmed:issn | 1557-7465 | lld:pubmed |
pubmed-article:20626297 | pubmed:author | pubmed-author:SuzukiYasuhir... | lld:pubmed |
pubmed-article:20626297 | pubmed:author | pubmed-author:KudoTomoyaT | lld:pubmed |
pubmed-article:20626297 | pubmed:author | pubmed-author:WangXishengX | lld:pubmed |
pubmed-article:20626297 | pubmed:author | pubmed-author:WenXiangshuX | lld:pubmed |
pubmed-article:20626297 | pubmed:author | pubmed-author:RodgersLaurel... | lld:pubmed |
pubmed-article:20626297 | pubmed:author | pubmed-author:PayneLauraL | lld:pubmed |
pubmed-article:20626297 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20626297 | pubmed:volume | 30 | lld:pubmed |
pubmed-article:20626297 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20626297 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20626297 | pubmed:pagination | 653-60 | lld:pubmed |
pubmed-article:20626297 | pubmed:dateRevised | 2011-9-13 | lld:pubmed |
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pubmed-article:20626297 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20626297 | pubmed:articleTitle | Predominant interferon-?-mediated expression of CXCL9, CXCL10, and CCL5 proteins in the brain during chronic infection with Toxoplasma gondii in BALB/c mice resistant to development of toxoplasmic encephalitis. | lld:pubmed |
pubmed-article:20626297 | pubmed:affiliation | Department of Biomedical Sciences and Pathobiology, Center for Molecular Medicine and Infectious Diseases, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA. | lld:pubmed |
pubmed-article:20626297 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20626297 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:20626297 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |