pubmed-article:9973398 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9973398 | lifeskim:mentions | umls-concept:C0003315 | lld:lifeskim |
pubmed-article:9973398 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:9973398 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
pubmed-article:9973398 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
pubmed-article:9973398 | lifeskim:mentions | umls-concept:C0205369 | lld:lifeskim |
pubmed-article:9973398 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:9973398 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:9973398 | pubmed:dateCreated | 1999-4-13 | lld:pubmed |
pubmed-article:9973398 | pubmed:abstractText | Autocrine interaction of Fas and Fas ligand leads to apoptosis of activated T cells, a process that is critical for the maintenance of peripheral T cell tolerance. Paracrine interactions of Fas ligand with T cells also may play an important role in the maintenance of tolerance, as Fas ligand can create immune-privileged sites and prevent graft rejection by inducing apoptosis in T cells. We surmised that APCs that express Fas ligand might directly induce apoptosis of T cells during presentation of Ag to the T cells, thus inducing Ag-specific, systemic T cell tolerance. Here, we show that profound, specific T cell unresponsiveness to alloantigen was induced by treatment of H-2k mice with H-2b APCs that expressed Fas ligand and that profound T cell unresponsiveness specific for the H-Y Ag was induced by treatment of H-2Db/H-Y TCR transgenic female mice with H-2Db/H-Y APCs that expressed Fas ligand. The induction of this systemic T cell tolerance required the expression of Fas ligand on the APCs as well as the expression of Fas on the T cells. The tolerance was restricted to the Ag presented by the APCs. The rapid and profound clonal deletion of the Ag-specific, peripheral T cells mediated by the Fas ligand-expressing APCs contributed to the induction of tolerance. These findings demonstrate that Ag-specific T cell tolerance can be induced by APCs that express Fas ligand and suggest a novel function for APCs in the induction of T cell apoptosis. Furthermore, they indicate a novel immunointervention strategy for treatment of graft rejection and autoantigen-specific autoimmune diseases. | lld:pubmed |
pubmed-article:9973398 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:language | eng | lld:pubmed |
pubmed-article:9973398 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9973398 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9973398 | pubmed:month | Feb | lld:pubmed |
pubmed-article:9973398 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:LieTT | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:LiuWW | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:WangZZ | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:MountzJ DJD | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:UINN | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:YangPP | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:ZhangH GHG | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:ZhouTT | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:BluethmannHH | lld:pubmed |
pubmed-article:9973398 | pubmed:author | pubmed-author:EdwardsC KCK | lld:pubmed |
pubmed-article:9973398 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9973398 | pubmed:day | 1 | lld:pubmed |
pubmed-article:9973398 | pubmed:volume | 162 | lld:pubmed |
pubmed-article:9973398 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9973398 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9973398 | pubmed:pagination | 1423-30 | lld:pubmed |
pubmed-article:9973398 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:9973398 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:9973398 | pubmed:articleTitle | Induction of specific T cell tolerance by Fas ligand-expressing antigen-presenting cells. | lld:pubmed |
pubmed-article:9973398 | pubmed:affiliation | Division of Clinical Immunology and Rheumatology, University of Alabama, Birmingham, AL 35294, USA. | lld:pubmed |
pubmed-article:9973398 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9973398 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9973398 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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