pubmed-article:9858515 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9858515 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
pubmed-article:9858515 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:9858515 | lifeskim:mentions | umls-concept:C0017263 | lld:lifeskim |
pubmed-article:9858515 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
pubmed-article:9858515 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:9858515 | pubmed:issue | 12 | lld:pubmed |
pubmed-article:9858515 | pubmed:dateCreated | 1999-1-22 | lld:pubmed |
pubmed-article:9858515 | pubmed:abstractText | The dysregulated expression of interleukin 4 (IL-4) can have deleterious effects on the outcome of infectious and allergic diseases. Despite this, the mechanisms by which naive T cells commit to IL-4 expression during differentiation into mature effector cells remain incompletely defined. As compared to cells from most strains of mice, activated CD4(+) T cells from BALB mice show a bias towards IL-4 production and T helper 2 commitment in vitro and in vivo. Here, we show that this bias arises not from an increase in the amount of IL-4 produced per cell, but rather from an increase in the proportion of CD4(+) T cells that commit to IL-4 expression. This strain-specific difference in commitment was independent of signals mediated via the IL-4 receptor and hence occurred upstream of potential autoregulatory effects of IL-4. Segregation analysis of the phenotype in an experimental backcross cohort implicated a polymorphic locus on chromosome 16. Consistent with a role in differentiation, expression of the phenotype was CD4(+) T cell intrinsic and was evident as early as 16 h after the activation of naive T cells. Probabilistic gene activation is proposed as a T cell-intrinsic mechanism capable of modulating the proportion of naive T cells that commit to IL-4 production. | lld:pubmed |
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pubmed-article:9858515 | pubmed:language | eng | lld:pubmed |
pubmed-article:9858515 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9858515 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9858515 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9858515 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9858515 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9858515 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9858515 | pubmed:month | Dec | lld:pubmed |
pubmed-article:9858515 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:9858515 | pubmed:author | pubmed-author:BixMM | lld:pubmed |
pubmed-article:9858515 | pubmed:author | pubmed-author:LocksleyR MRM | lld:pubmed |
pubmed-article:9858515 | pubmed:author | pubmed-author:SchorkN JNJ | lld:pubmed |
pubmed-article:9858515 | pubmed:author | pubmed-author:WenkV AVA | lld:pubmed |
pubmed-article:9858515 | pubmed:author | pubmed-author:ThielBB | lld:pubmed |
pubmed-article:9858515 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9858515 | pubmed:day | 21 | lld:pubmed |
pubmed-article:9858515 | pubmed:volume | 188 | lld:pubmed |
pubmed-article:9858515 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9858515 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9858515 | pubmed:pagination | 2289-99 | lld:pubmed |
pubmed-article:9858515 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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