pubmed-article:9353008 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9353008 | lifeskim:mentions | umls-concept:C0123759 | lld:lifeskim |
pubmed-article:9353008 | lifeskim:mentions | umls-concept:C0020964 | lld:lifeskim |
pubmed-article:9353008 | lifeskim:mentions | umls-concept:C0023276 | lld:lifeskim |
pubmed-article:9353008 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:9353008 | pubmed:dateCreated | 1997-11-13 | lld:pubmed |
pubmed-article:9353008 | pubmed:abstractText | Interleukin-12 (IL-12)-deficient mice derived from a strain genetically resistant to infection with Leishmania major were recently shown to be susceptible toward this parasite, developing a strong Th2 response after injection of a large number of parasites. We further investigated the role of IL-12 in L. major infection by studying the responses of mutant mice against smaller numbers of parasites. IL-12-deficient mice infected with only small numbers of parasites showed the progressive lesion development and high parasite burden associated with a polarized Th2 response. Our data show that IL-12 is indispensable for protective immunity against L. major. Even at low inocula, no salvage pathway appears to compensate for the lack of IL-12. However, genetically susceptible BALB/c mice infected with small numbers of parasites were able to resolve lesions and restrict the parasite burden to levels which were 10(5)-fold lower than those in IL-12-deficient mice. In contrast to mutant mice, BALB/c mice mounted a type 1 response against low inocula of L. major. IL-12-deficient BALB/c mice, however, developed a type 2 response. These data emphasize the essential role of IL-12 in resistance against L. major. In addition, this study suggests that in the absence of IL-12, susceptibility to L. major is determined by the inability to induce a Th1 response rather than the development of a Th2 response. Our results are relevant for potential vaccination strategies that use low inocula of infective microorganisms which fail to induce a protective type 1 response at higher inocula. | lld:pubmed |
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pubmed-article:9353008 | pubmed:language | eng | lld:pubmed |
pubmed-article:9353008 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9353008 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9353008 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9353008 | pubmed:month | Nov | lld:pubmed |
pubmed-article:9353008 | pubmed:issn | 0019-9567 | lld:pubmed |
pubmed-article:9353008 | pubmed:author | pubmed-author:AlberGG | lld:pubmed |
pubmed-article:9353008 | pubmed:author | pubmed-author:MattnerFF | lld:pubmed |
pubmed-article:9353008 | pubmed:author | pubmed-author:Di PadovaKK | lld:pubmed |
pubmed-article:9353008 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9353008 | pubmed:volume | 65 | lld:pubmed |
pubmed-article:9353008 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9353008 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9353008 | pubmed:pagination | 4378-83 | lld:pubmed |
pubmed-article:9353008 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:9353008 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9353008 | pubmed:articleTitle | Interleukin-12 is indispensable for protective immunity against Leishmania major. | lld:pubmed |
pubmed-article:9353008 | pubmed:affiliation | Department of Infectious Diseases, F. Hoffmann-La Roche AG, Basel, Switzerland. | lld:pubmed |
pubmed-article:9353008 | pubmed:publicationType | Journal Article | lld:pubmed |
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