pubmed-article:12811839 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C0023283 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C0021747 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C0020964 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C1415900 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C0086982 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
pubmed-article:12811839 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
pubmed-article:12811839 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:12811839 | pubmed:dateCreated | 2003-6-17 | lld:pubmed |
pubmed-article:12811839 | pubmed:abstractText | Although STAT1-dependent signaling mediates biological functions of IFN-alpha/beta and IFN-gamma, recent reports indicate that STAT1-independent IFN signaling also regulates expression of several genes. To determine the roles of STAT1-dependent and -independent IFN signaling in the regulation of immunity during cutaneous leishmaniasis, we studied the course of Leishmania major infection in resistant C57BL/6 mice lacking the STAT1 gene. While L. major-infected STAT1(+/+) mice resolved their lesions, STAT1(-/-) mice developed large lesions containing significantly more parasites. Moreover, the inability of STAT1(-/-) mice to control L. major infection was due to the lack of Th1 development associated with reduced production of IL-12, IFN-gamma and nitric oxide. Although STAT1(-/-) mice produced more IL-4 and total IgE than STAT1(+/+) mice later during infection, these differences were not significant. Nevertheless, at these time points lymph node cells from STAT1(-/-) mice produced significantly more IL-10. Finally, STAT1(-/-) mice were also susceptible to low dose L. major infection. Thesefindings demonstrate that STAT1-mediated IFN signaling is indispensable for the development of protective immunity against cutaneous L. major infection. Moreover, they also suggest that the protective role of STAT1-mediated signaling is due to its ability to induce Th1 development during infection with this parasite. | lld:pubmed |
pubmed-article:12811839 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:language | eng | lld:pubmed |
pubmed-article:12811839 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:12811839 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12811839 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12811839 | pubmed:month | Jul | lld:pubmed |
pubmed-article:12811839 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:12811839 | pubmed:author | pubmed-author:SatoskarAbhay... | lld:pubmed |
pubmed-article:12811839 | pubmed:author | pubmed-author:RosasLucia... | lld:pubmed |
pubmed-article:12811839 | pubmed:author | pubmed-author:DurbinJoanJ | lld:pubmed |
pubmed-article:12811839 | pubmed:author | pubmed-author:KeiserTracyT | lld:pubmed |
pubmed-article:12811839 | pubmed:author | pubmed-author:PylesRyanR | lld:pubmed |
pubmed-article:12811839 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12811839 | pubmed:volume | 33 | lld:pubmed |
pubmed-article:12811839 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12811839 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12811839 | pubmed:pagination | 1799-805 | lld:pubmed |
pubmed-article:12811839 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
pubmed-article:12811839 | pubmed:meshHeading | pubmed-meshheading:12811839... | lld:pubmed |
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pubmed-article:12811839 | pubmed:meshHeading | pubmed-meshheading:12811839... | lld:pubmed |
pubmed-article:12811839 | pubmed:meshHeading | pubmed-meshheading:12811839... | lld:pubmed |
pubmed-article:12811839 | pubmed:meshHeading | pubmed-meshheading:12811839... | lld:pubmed |
pubmed-article:12811839 | pubmed:meshHeading | pubmed-meshheading:12811839... | lld:pubmed |
pubmed-article:12811839 | pubmed:year | 2003 | lld:pubmed |
pubmed-article:12811839 | pubmed:articleTitle | Development of protective immunity against cutaneous leishmaniasis is dependent on STAT1-mediated IFN signaling pathway. | lld:pubmed |
pubmed-article:12811839 | pubmed:affiliation | Department of Microbiology, The Ohio State University, 484 West 12th Avenue, Columbus, OH 43210, USA. | lld:pubmed |
pubmed-article:12811839 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12811839 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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