| pubmed-article:12036882 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12036882 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:12036882 | lifeskim:mentions | umls-concept:C0382839 | lld:lifeskim |
| pubmed-article:12036882 | lifeskim:mentions | umls-concept:C1457869 | lld:lifeskim |
| pubmed-article:12036882 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:12036882 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:12036882 | pubmed:dateCreated | 2002-5-30 | lld:pubmed |
| pubmed-article:12036882 | pubmed:abstractText | T-cell responses are regulated by activating and inhibiting signals. CD28 and its homologue, cytotoxic T-lymphocyte antigen 4 (CTLA-4), are the primary regulatory molecules that enhance or inhibit T-cell activation, respectively. Recently it has been shown that inhibitory natural killer (NK) cell receptors (NKRs) are expressed on subsets of T cells. It has been proposed that these receptors may also play an important role in regulating T-cell responses. However, the extent to which the NKRs modulate peripheral T-cell homeostasis and activation in vivo remains unclear. In this report we show that NK cell inhibitory receptor Ly49A engagement on T cells dramatically limits T-cell activation and the resultant lymphoproliferative disorder that occurs in CTLA-4-deficient mice. Prevention of activation and expansion of the potentially autoreactive CTLA-4(-/-) T cells by the Ly49A-mediated inhibitory signal demonstrates that NKR expression can play an important regulatory role in T-cell homeostasis in vivo. These results demonstrate the importance of inhibitory signals in T-cell homeostasis and suggest the common biochemical basis of inhibitory signaling pathways in T lymphocytes. | lld:pubmed |
| pubmed-article:12036882 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12036882 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12036882 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12036882 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:12036882 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:12036882 | pubmed:author | pubmed-author:RauletDavid... | lld:pubmed |
| pubmed-article:12036882 | pubmed:author | pubmed-author:AllisonJames... | lld:pubmed |
| pubmed-article:12036882 | pubmed:author | pubmed-author:HeldWernerW | lld:pubmed |
| pubmed-article:12036882 | pubmed:author | pubmed-author:ChambersCynth... | lld:pubmed |
| pubmed-article:12036882 | pubmed:author | pubmed-author:KangJoonsooJ | lld:pubmed |
| pubmed-article:12036882 | pubmed:author | pubmed-author:WuYongjianY | lld:pubmed |
| pubmed-article:12036882 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12036882 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12036882 | pubmed:volume | 99 | lld:pubmed |
| pubmed-article:12036882 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12036882 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12036882 | pubmed:pagination | 4509-16 | lld:pubmed |
| pubmed-article:12036882 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:12036882 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12036882 | pubmed:articleTitle | The lymphoproliferative defect in CTLA-4-deficient mice is ameliorated by an inhibitory NK cell receptor. | lld:pubmed |
| pubmed-article:12036882 | pubmed:affiliation | Department of Pathology, University of Massachusetts Medical School, Worcester, 01655, USA. cynthia.chambers@umassmed.edu | lld:pubmed |
| pubmed-article:12036882 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12036882 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12036882 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:12477 | entrezgene:pubmed | pubmed-article:12036882 | lld:entrezgene |
| entrez-gene:16627 | entrezgene:pubmed | pubmed-article:12036882 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:12036882 | lld:entrezgene |
