| pubmed-article:8584935 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8584935 | lifeskim:mentions | umls-concept:C0023270 | lld:lifeskim |
| pubmed-article:8584935 | lifeskim:mentions | umls-concept:C0123759 | lld:lifeskim |
| pubmed-article:8584935 | lifeskim:mentions | umls-concept:C0242632 | lld:lifeskim |
| pubmed-article:8584935 | lifeskim:mentions | umls-concept:C0314657 | lld:lifeskim |
| pubmed-article:8584935 | lifeskim:mentions | umls-concept:C0815089 | lld:lifeskim |
| pubmed-article:8584935 | pubmed:issue | 5251 | lld:pubmed |
| pubmed-article:8584935 | pubmed:dateCreated | 1996-3-21 | lld:pubmed |
| pubmed-article:8584935 | pubmed:abstractText | The genetic background of T lymphocytes influences development of the T helper (TH) phenotype, resulting in either resistance or susceptibility of certain mouse strains to pathogens such as Leishmania major. With an in vitro model system, a difference in maintenance of responsiveness of T cells to interleukin-12 (IL-12) was detected between BALB/c and B10.D2 mice. Although naive T cells from both strains initially responded to IL-12, BALB/c T cells lost IL-12 responsiveness after stimulation with antigen in vitro, even when cocultured with B10.D2 T cells. Thus, susceptibility of BALB/c mice to infection with L. major may derive from the loss of the ability to generate IL-12-induced TH1 responses rather than from an IL-4-induced TH2 response. | lld:pubmed |
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| pubmed-article:8584935 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8584935 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8584935 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8584935 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8584935 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:8584935 | pubmed:issn | 0036-8075 | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:MurphyK MKM | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:HsiehC SCS | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:SteenR GRG | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:GorhamJ DJD | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:DietrichW FWF | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:GülerM LML | lld:pubmed |
| pubmed-article:8584935 | pubmed:author | pubmed-author:MackeyA JAJ | lld:pubmed |
| pubmed-article:8584935 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8584935 | pubmed:day | 16 | lld:pubmed |
| pubmed-article:8584935 | pubmed:volume | 271 | lld:pubmed |
| pubmed-article:8584935 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8584935 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8584935 | pubmed:pagination | 984-7 | lld:pubmed |
| pubmed-article:8584935 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8584935 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8584935 | pubmed:articleTitle | Genetic susceptibility to Leishmania: IL-12 responsiveness in TH1 cell development. | lld:pubmed |
| pubmed-article:8584935 | pubmed:affiliation | Department of Pathology, Washington University School of Medicine, St. Louis, MO 63110, USA. | lld:pubmed |
| pubmed-article:8584935 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8584935 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:8584935 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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