| pubmed-article:10899917 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C0003320 | lld:lifeskim |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C0039198 | lld:lifeskim |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C1334114 | lld:lifeskim |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C0205470 | lld:lifeskim |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C1314677 | lld:lifeskim |
| pubmed-article:10899917 | lifeskim:mentions | umls-concept:C1511636 | lld:lifeskim |
| pubmed-article:10899917 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:10899917 | pubmed:dateCreated | 2000-8-10 | lld:pubmed |
| pubmed-article:10899917 | pubmed:abstractText | This report shows that cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) plays a key role in T cell-mediated dominant immunologic self-tolerance. In vivo blockade of CTLA-4 for a limited period in normal mice leads to spontaneous development of chronic organ-specific autoimmune diseases, which are immunopathologically similar to human counterparts. In normal naive mice, CTLA-4 is constitutively expressed on CD25(+)CD4(+) T cells, which constitute 5-10% of peripheral CD4(+) T cells. When the CD25(+)CD4(+) T cells are stimulated via the T cell receptor in vitro, they potently suppress antigen-specific and polyclonal activation and proliferation of other T cells, including CTLA-4-deficient T cells, and blockade of CTLA-4 abrogates the suppression. CD28-deficient CD25(+)CD4(+) T cells can also suppress normal T cells, indicating that CD28 is dispensable for activation of the regulatory T cells. Thus, the CD25(+)CD4(+) regulatory T cell population engaged in dominant self-tolerance may require CTLA-4 but not CD28 as a costimulatory molecule for its functional activation. Furthermore, interference with this role of CTLA-4 suffices to elicit autoimmune disease in otherwise normal animals, presumably through affecting CD25(+)CD4(+) T cell-mediated control of self-reactive T cells. This unique function of CTLA-4 could be exploited to potentiate T cell-mediated immunoregulation, and thereby to induce immunologic tolerance or to control autoimmunity. | lld:pubmed |
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| pubmed-article:10899917 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:10899917 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10899917 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10899917 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:10899917 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:TakahashiTT | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:UedaHH | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:MaoT STS | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:YamazakiSS | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:SakaguchiSS | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:ShimizuJJ | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:SakaguchiNN | lld:pubmed |
| pubmed-article:10899917 | pubmed:author | pubmed-author:TagamiTT | lld:pubmed |
| pubmed-article:10899917 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10899917 | pubmed:day | 17 | lld:pubmed |
| pubmed-article:10899917 | pubmed:volume | 192 | lld:pubmed |
| pubmed-article:10899917 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10899917 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10899917 | pubmed:pagination | 303-10 | lld:pubmed |
| pubmed-article:10899917 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:10899917 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10899917 | pubmed:articleTitle | Immunologic self-tolerance maintained by CD25(+)CD4(+) regulatory T cells constitutively expressing cytotoxic T lymphocyte-associated antigen 4. | lld:pubmed |
| pubmed-article:10899917 | pubmed:affiliation | Department of Experimental Pathology, Institute for Frontier Medical Sciences, Kyoto University, Kyoto 606-8507, Japan. | lld:pubmed |
| pubmed-article:10899917 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10899917 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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