| pubmed-article:9096368 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C0205615 | lld:lifeskim |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:9096368 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:9096368 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:9096368 | pubmed:dateCreated | 1997-5-8 | lld:pubmed |
| pubmed-article:9096368 | pubmed:abstractText | CD4+ T cells from T cell receptor transgenic mice that have been vigorously primed to be interleukin (IL)-4 producers (T(H2) cells) are capable of producing IL-4 even if restimulated in the absence of IL-4 and in the presence of IL-12. T cells vigorously primed in the absence of IL-4 (T(H1) cells) fail to produce IL-4 even if restimulated under conditions that would cause a naive T cell to produce IL-4. In contrast, interferon gamma (IFN-gamma) production is highly cytokine-regulated. T cells primed in the presence of IL-4 develop into IFN-gamma producers if IFN-gamma is included in the priming culture and if the cells are challenged in the presence of IL-12, presumably reflecting the role of IFN-gamma in inducing responsiveness to IL-12. Cells primed in the absence of IL-4 become highly responsive to IL-12 if IFN-gamma is included in the priming culture, and these cells are excellent IFN-gamma producers upon challenge; IL-12 considerably enhances their production of IFN-gamma. If cells are primed in the absence of IL-4 and IFN-gamma, they show very weak responsiveness to IL-12 as determined by STAT-4 activation. However, these cells acquire IL-12 responsiveness if cultured with IFN-gamma for a period as short as 4 hr. Thereafter, they produce large amounts of IFN-gamma upon challenge with antigen in the presence of IL-12. These results indicate that in primed CD4+ T cells, IL-4 production is largely cytokine-autonomous, whereas IFN-gamma production is highly cytokine-regulated. | lld:pubmed |
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| pubmed-article:9096368 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9096368 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9096368 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9096368 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9096368 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:9096368 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:9096368 | pubmed:author | pubmed-author:REESW HWH | lld:pubmed |
| pubmed-article:9096368 | pubmed:author | pubmed-author:PaulW EWE | lld:pubmed |
| pubmed-article:9096368 | pubmed:author | pubmed-author:HuangHH | lld:pubmed |
| pubmed-article:9096368 | pubmed:author | pubmed-author:Hu-LiJJ | lld:pubmed |
| pubmed-article:9096368 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9096368 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:9096368 | pubmed:volume | 94 | lld:pubmed |
| pubmed-article:9096368 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9096368 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9096368 | pubmed:pagination | 3189-94 | lld:pubmed |
| pubmed-article:9096368 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9096368 | pubmed:meshHeading | pubmed-meshheading:9096368-... | lld:pubmed |
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| pubmed-article:9096368 | pubmed:meshHeading | pubmed-meshheading:9096368-... | lld:pubmed |
| pubmed-article:9096368 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9096368 | pubmed:articleTitle | In differentiated CD4+ T cells, interleukin 4 production is cytokine-autonomous, whereas interferon gamma production is cytokine-dependent. | lld:pubmed |
| pubmed-article:9096368 | pubmed:affiliation | Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1892, USA. | lld:pubmed |
| pubmed-article:9096368 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9096368 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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