| pubmed-article:8932763 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C1521751 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C0443199 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C1149404 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C0023276 | lld:lifeskim |
| pubmed-article:8932763 | lifeskim:mentions | umls-concept:C0205251 | lld:lifeskim |
| pubmed-article:8932763 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8932763 | pubmed:dateCreated | 1996-12-12 | lld:pubmed |
| pubmed-article:8932763 | pubmed:abstractText | In murine cutaneous leishmaniasis caused by Leishmania major (Lm), resistance often associates with the outgrowth of Lm-specific Th1 cells. Parasites are eliminated by Th1-mediated activation of infected macrophages (M phi) which destroy Lm by producing toxic nitrogen and oxygen radicals. The cytokine IFN-alpha activates microbicidal functions of M phis and facilitates outgrowth of Th1 cells. Therefore, we compared the course of infection with Lm in resistant C57BL/6 mice, bearing the If-1h high expression allele for IFN-alpha/beta, with the congenic B6.C-H-28c mouse, bearing the If-1I low expression allele from the Lm-susceptible BALB/c strain. We observed that B6.C-H-28c animals developed up to 70% larger footpad lesions and harbored up to 1000-fold more parasites than C57BL/6 mice. Furthermore, peak Lm-specific IFN-gamma production in the B6.C-H-28c animals was lower and delayed by approximately 2 weeks, whereas IL-4 production was higher and persisted approximately 2 weeks longer. Since these results suggested that IFN-alpha/beta plays a protective role in mice infected with Lm, we determined whether infusing B6.C-H-28c mice with IFN-alpha would influence the course of infection with Lm. Unfortunately, the mice developed severe peritoneal hemorrhaging in response to injection with IFN-alpha. Therefore, we examined the ability of IFN-alpha to activate M phis to destroy Lm in vitro. We observed that rIFN-alpha could synergize with subactivating doses of LPS to activate both C57BL/6 and BALB/c peritoneal M phis to produce NO and to kill intracellular Lm. Taken as a whole, these results suggest that type I interferons may play a protective role in cutaneous leishmaniasis. | lld:pubmed |
| pubmed-article:8932763 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8932763 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8932763 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8932763 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8932763 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:8932763 | pubmed:issn | 0014-4894 | lld:pubmed |
| pubmed-article:8932763 | pubmed:author | pubmed-author:MorioSS | lld:pubmed |
| pubmed-article:8932763 | pubmed:author | pubmed-author:TitusR GRG | lld:pubmed |
| pubmed-article:8932763 | pubmed:author | pubmed-author:ShankarA HAH | lld:pubmed |
| pubmed-article:8932763 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8932763 | pubmed:volume | 84 | lld:pubmed |
| pubmed-article:8932763 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8932763 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8932763 | pubmed:pagination | 136-43 | lld:pubmed |
| pubmed-article:8932763 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
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| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
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| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:meshHeading | pubmed-meshheading:8932763-... | lld:pubmed |
| pubmed-article:8932763 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8932763 | pubmed:articleTitle | Leishmania major: differential resistance to infection in C57BL/6 (high interferon-alpha/beta) and congenic B6.C-H-28c (low interferon-alpha/beta) mice. | lld:pubmed |
| pubmed-article:8932763 | pubmed:affiliation | Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:8932763 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8932763 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:8932763 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8932763 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8932763 | lld:pubmed |
