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rdf:type |
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lifeskim:mentions |
umls-concept:C0007589,
umls-concept:C0038856,
umls-concept:C0085358,
umls-concept:C1332399,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1511938,
umls-concept:C1514873,
umls-concept:C1519595,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1706438,
umls-concept:C2698600
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pubmed:issue |
10
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pubmed:dateCreated |
2010-11-4
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pubmed:databankReference |
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pubmed:abstractText |
Ig-like transcript 3 (ILT3) is an inhibitory receptor expressed by tolerogenic dendritic cells. When human CD8(+) T cells are allostimulated in the presence of recombinant ILT3-Fc protein, they differentiate into antigenic specific T suppressor (Ts) cells that inhibit CD4 and CD8 T cell effector function both in vitro and in vivo. ILT3-Fc-induced CD8(+) Ts cells express high amounts of BCL6 that are crucial to their function. Knockdown of BCL6 from unprimed human T cells prevents their differentiation into Ts cells, whereas ex vivo overexpression of BCL6 converts CD8(+) T cells into Ts cells. NOD/SCID mice transplanted with human pancreatic islets and humanized by injection of human PBMCs tolerate the graft and develop BCL6(high) CD8(+) Ts cells when treated with ILT3-Fc before or after the onset of rejection. This indicates that ILT3-Fc acts through BCL6 and is a potent immunosuppressive agent for reversing the onset of allo- or possibly autoimmune attacks against pancreatic islets.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
|
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1550-6606
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pubmed:author |
pubmed-author:ChangChih-ChaoCC,
pubmed-author:CortesiniRaffaelloR,
pubmed-author:D'AgatiVivette DVD,
pubmed-author:HoEric KEK,
pubmed-author:LiuZhuoruZ,
pubmed-author:StokesMichael BMB,
pubmed-author:Suciu-FocaNicoleN,
pubmed-author:TorkamaniAli AAA,
pubmed-author:VladGeorgeG,
pubmed-author:WitkowskiPiotrP,
pubmed-author:ZhangQing-yinQY
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
185
|
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pubmed:owner |
NLM
|
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5714-22
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pubmed:meshHeading |
pubmed-meshheading:20935202-Animals,
pubmed-meshheading:20935202-CD8-Positive T-Lymphocytes,
pubmed-meshheading:20935202-Cell Differentiation,
pubmed-meshheading:20935202-DNA-Binding Proteins,
pubmed-meshheading:20935202-Female,
pubmed-meshheading:20935202-Gene Knockdown Techniques,
pubmed-meshheading:20935202-Graft Rejection,
pubmed-meshheading:20935202-Humans,
pubmed-meshheading:20935202-Immunoglobulin Fc Fragments,
pubmed-meshheading:20935202-Immunohistochemistry,
pubmed-meshheading:20935202-Islets of Langerhans Transplantation,
pubmed-meshheading:20935202-Mice,
pubmed-meshheading:20935202-Mice, Inbred NOD,
pubmed-meshheading:20935202-Mice, SCID,
pubmed-meshheading:20935202-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:20935202-Receptors, Cell Surface,
pubmed-meshheading:20935202-Recombinant Fusion Proteins,
pubmed-meshheading:20935202-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:20935202-Transfection,
pubmed-meshheading:20935202-Transplantation Tolerance
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pubmed:year |
2010
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pubmed:articleTitle |
BCL6 is required for differentiation of Ig-like transcript 3-Fc-induced CD8+ T suppressor cells.
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pubmed:affiliation |
Department of Pathology and Cell Biology, Columbia University, New York, NY 10032, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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