| pubmed-article:15494488 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C0003069 | lld:lifeskim |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C0111208 | lld:lifeskim |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:15494488 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:15494488 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:15494488 | pubmed:dateCreated | 2004-10-20 | lld:pubmed |
| pubmed-article:15494488 | pubmed:abstractText | IL-2-deficient mice develop a lymphoproliferative and autoimmune disease characterized by autoimmune hemolytic anemia (AHA) and inflammatory bowel disease. We have previously reported that IL-2 is necessary for optimal up-regulation of CTLA-4, an inducible negative regulator of T cell activation. In this study, we have tested the hypothesis that reduced expression of CTLA-4 in IL-2-deficient T cells contributes to the pathogenesis of disease in IL-2-deficient mice. Expression of CTLA-4 as a transgene completely prevented lymphoaccumulation and AHA in IL-2-deficient mice. The normalization of T cell numbers was due to inhibition of expansion of conventional CD4+CD25- T cells rather than to rescue of the numbers or function of CD4+CD25+ regulatory T cells, suggesting that CTLA-4 expression on conventional T cells plays a role in maintaining normal T cell homeostasis. In addition, the inhibitory effect of the CTLA-4 transgene on T cell expansion was at least in part independent of CD28 expression. Our results suggest that deficient CTLA-4 expression on conventional T cells contributes to the pathophysiology of the lymphoproliferative disease and AHA in IL-2-deficient mice. Thus, restoring CTLA-4 expression in T cells may be an attractive strategy to control clinical autoimmune diseases in which CTLA-4 expression is reduced. | lld:pubmed |
| pubmed-article:15494488 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15494488 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15494488 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:15494488 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15494488 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15494488 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:15494488 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15494488 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15494488 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:15494488 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:HwangKwang... | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:SweattWilliam... | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:AlegreMaria-L... | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:PaluckiDavid... | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:ChuangEllenE | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:MashayekhiMon... | lld:pubmed |
| pubmed-article:15494488 | pubmed:author | pubmed-author:SattarHussain... | lld:pubmed |
| pubmed-article:15494488 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15494488 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:15494488 | pubmed:volume | 173 | lld:pubmed |
| pubmed-article:15494488 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15494488 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15494488 | pubmed:pagination | 5415-24 | lld:pubmed |
| pubmed-article:15494488 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:15494488 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15494488 | pubmed:articleTitle | Transgenic expression of CTLA-4 controls lymphoproliferation in IL-2-deficient mice. | lld:pubmed |
| pubmed-article:15494488 | pubmed:affiliation | Section of Rheumatology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA. | lld:pubmed |
| pubmed-article:15494488 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15494488 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15494488 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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