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rdf:type |
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lifeskim:mentions |
umls-concept:C0014597,
umls-concept:C0017262,
umls-concept:C0022077,
umls-concept:C0031916,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0111208,
umls-concept:C0301625,
umls-concept:C1155065,
umls-concept:C1171362,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1515670,
umls-concept:C1706438,
umls-concept:C1947978,
umls-concept:C2348867,
umls-concept:C2698599,
umls-concept:C2698600
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pubmed:issue |
7
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pubmed:dateCreated |
2004-3-22
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pubmed:abstractText |
Pigment epithelial (PE) cells cultured from the eye possess the novel property of suppressing TCR-dependent activation of T cells in vitro. Iris PE (IPE) cells accomplish this suppression by a direct cell contact mechanism in which B7-2 expressed by the PE cells interacts with CTLA-4 on responding T cells. Because CTLA-4 expression is constitutively expressed on a very small proportion of naive splenic T cells and since exposure of splenic T cells to IPE leads to global T cell suppression, we have inquired into the mechanism by which suppression is achieved. Using splenic T cells and IPE from donor mice with disrupted genes for CD80 (B7-1), CD86 (B7-2), CTLA-4, and/or CD28, we report that B7-2(+) IPE in the presence of anti-CD3 supported selectively the activation of CTLA-4(+) CD8(+) T cells that express their own B7-2 and secrete enhanced amounts of active TGFbeta. By contrast, activation of CTLA-4-negative T cells, especially CD4(+) cells, in these cultures was profoundly suppressed. Because global suppression of T cell activation in these cultures was obtained only when both IPE and T cells possessed B7-2 genes and expressed the costimulators as surface molecules, we propose that T cells activated in the presence of parenchymal cells from the eye (an immune privileged site) express B7-2 in a manner that equips them to suppress bystander T cells. Thus, B7-2 expression on T cells participates in their eventual ability to function as regulators in vitro.
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pubmed:grant |
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/BTLA protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
172
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4184-94
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15034031-Animals,
pubmed-meshheading:15034031-Antigens, CD,
pubmed-meshheading:15034031-Antigens, CD3,
pubmed-meshheading:15034031-Antigens, CD86,
pubmed-meshheading:15034031-Antigens, Differentiation,
pubmed-meshheading:15034031-Bystander Effect,
pubmed-meshheading:15034031-CD4-Positive T-Lymphocytes,
pubmed-meshheading:15034031-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15034031-CTLA-4 Antigen,
pubmed-meshheading:15034031-Cell Division,
pubmed-meshheading:15034031-Cells, Cultured,
pubmed-meshheading:15034031-Cytokines,
pubmed-meshheading:15034031-Immune Sera,
pubmed-meshheading:15034031-Iris,
pubmed-meshheading:15034031-Lymphocyte Activation,
pubmed-meshheading:15034031-Membrane Glycoproteins,
pubmed-meshheading:15034031-Mice,
pubmed-meshheading:15034031-Mice, Inbred C57BL,
pubmed-meshheading:15034031-Mice, Knockout,
pubmed-meshheading:15034031-Pigment Epithelium of Eye,
pubmed-meshheading:15034031-Receptors, Immunologic,
pubmed-meshheading:15034031-T-Lymphocytes, Regulatory
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pubmed:year |
2004
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pubmed:articleTitle |
CTLA-4+CD8+ T cells that encounter B7-2+ iris pigment epithelial cells express their own B7-2 to achieve global suppression of T cell activation.
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pubmed:affiliation |
Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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