| pubmed-article:15343366 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15343366 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:15343366 | lifeskim:mentions | umls-concept:C0020964 | lld:lifeskim |
| pubmed-article:15343366 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:15343366 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:15343366 | pubmed:dateCreated | 2004-9-2 | lld:pubmed |
| pubmed-article:15343366 | pubmed:abstractText | Interleukin-2 (IL-2) was identified based on its potent T-cell growth-factor activity and is widely considered to be a key cytokine in T-cell-dependent immune responses. However, the main non-redundant activity of this cytokine centres on the regulation of T-cell tolerance, and recent studies indicate that a failure in the production of CD4(+)CD25(+) regulatory T cells is the underlying cause of autoimmunity in the absence of IL-2. In marked contrast to the importance of IL-2 in peripheral T-cell tolerance, T-cell immunity is readily elicited to various agents in the absence of IL-2 in vivo. Here, we discuss these findings and, in particular, the action of IL-2 on regulatory T cells and effector cells, and the targeting of IL-2 and/or the IL-2 receptor in clinical settings. | lld:pubmed |
| pubmed-article:15343366 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15343366 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15343366 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15343366 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15343366 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15343366 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15343366 | pubmed:issn | 1474-1733 | lld:pubmed |
| pubmed-article:15343366 | pubmed:author | pubmed-author:MalekThomas... | lld:pubmed |
| pubmed-article:15343366 | pubmed:author | pubmed-author:BayerAllison... | lld:pubmed |
| pubmed-article:15343366 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15343366 | pubmed:volume | 4 | lld:pubmed |
| pubmed-article:15343366 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15343366 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15343366 | pubmed:pagination | 665-74 | lld:pubmed |
| pubmed-article:15343366 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:meshHeading | pubmed-meshheading:15343366... | lld:pubmed |
| pubmed-article:15343366 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15343366 | pubmed:articleTitle | Tolerance, not immunity, crucially depends on IL-2. | lld:pubmed |
| pubmed-article:15343366 | pubmed:affiliation | Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, Florida 33136, USA. tmalek@med.miami.edu | lld:pubmed |
| pubmed-article:15343366 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15343366 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15343366 | pubmed:publicationType | Review | lld:pubmed |
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