| pubmed-article:2935591 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0596138 | lld:lifeskim |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:2935591 | lifeskim:mentions | umls-concept:C0205269 | lld:lifeskim |
| pubmed-article:2935591 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:2935591 | pubmed:dateCreated | 1986-3-26 | lld:pubmed |
| pubmed-article:2935591 | pubmed:abstractText | During the course of investigating the regulation of IL-2-dependent T cell proliferation, we found that the subset of human T cells expressing the T4 surface glycoprotein become refractory to IL-2 growth promotion earlier than T8+ cells. Since T4+ cells proliferate in an autocrine fashion to endogenous IL-2, whereas most T8+ cells respond in a paracrine fashion to IL-2 derived from T4+ cells, we thought it likely that a unique mechanism was operative to restrict T4+ cell IL-2-dependent autocrine proliferation. Moreover, we anticipated that the T4+ cell IL-2-refractory state related either to suppression by T8+ cells, or to expression of T4+ cell IL-2-R. However, several experimental approaches did not support either of these mechanisms as being responsible for the loss of T4+ cell IL-2 responsiveness. Isolated T4+ cells ceased to respond to IL-2 well before T8+ cells, and before the disappearance of adequate levels of IL-2-R. Moreover, a detailed comparison of IL-2-R expression by T4+ vs. T8+ cells revealed no differences in the number, affinity, rate of expression, or functional activity of high-affinity IL-2-R expressed by the two subsets. Accordingly, T4+ cell autocrine IL-2 responsiveness is restricted by a mechanism that is independent of IL-2-R, and which ultimately results in cessation of both T4+ and T8+ cell IL-2-dependent clonal expansion. | lld:pubmed |
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| pubmed-article:2935591 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2935591 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2935591 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2935591 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2935591 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:2935591 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:2935591 | pubmed:author | pubmed-author:SmithK AKA | lld:pubmed |
| pubmed-article:2935591 | pubmed:author | pubmed-author:GullbergMM | lld:pubmed |
| pubmed-article:2935591 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2935591 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:2935591 | pubmed:volume | 163 | lld:pubmed |
| pubmed-article:2935591 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2935591 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2935591 | pubmed:pagination | 270-84 | lld:pubmed |
| pubmed-article:2935591 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2935591 | pubmed:year | 1986 | lld:pubmed |
| pubmed-article:2935591 | pubmed:articleTitle | Regulation of T cell autocrine growth. T4+ cells become refractory to interleukin 2. | lld:pubmed |
| pubmed-article:2935591 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2935591 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2935591 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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