rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2005-7-12
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pubmed:abstractText |
Naturally arising CD4(+)CD25(+) regulatory T (T(R)) cells are engaged in the maintenance of self tolerance and prevention of autoimmune diseases. However, accumulating evidence suggests that a fraction of peripheral CD4(+)CD25(-) T cells also possesses regulatory activity. Programmed death-1 (PD-1) is a new member of the CD28/CTLA-4 family, which has been implicated in the maintenance of peripheral self tolerance. Here, we identified a subpopulation of CD4(+)CD25(-)PD-1(+) T cells in the spleen of naive mice that constitutively expressed CTLA-4 and FoxP3 and was hypoproliferative in response to anti-CD3 antibody stimulation in vitro. However, the CD4(+)CD25(-)PD-1(+) T cells uniquely produced large amounts of IL-4 and IL-10 in response to anti-CD3 and anti-CD28 mAb stimulation, unlike the CD4(+)CD25(+) T(R) cells. The CD4(+)CD25(-)PD-1(+) T cells exhibited a suppressor activity against the proliferation of anti-CD3 antibody-stimulated CD4(+)CD25(-)PD-1(-) T cells in vitro, which was partially abrogated by anti-CTLA-4 mAb, but not by anti-IL-10 or anti-PD-1 mAb. Remarkably, the CD4(+)CD25(-)PD-1(+) T cells inhibited the development of colitis induced by adoptive transfer of CD4(+)CD45RB(high) T cells into C.B17-scid/scid mice, albeit to a lesser extent than CD4(+)CD25(+) T(R) cells, in a CTLA-4-dependent manner. These results indicate that the CD4(+)CD25(-)PD-1(+) T cells contain substantial amounts of T(R) cells that are involved in the maintenance of peripheral tolerance.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Apoptosis Regulatory Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Pdcd1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Programmed Cell Death 1 Receptor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
|
pubmed:issn |
0014-2980
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pubmed:author |
pubmed-author:AkibaHisayaH,
pubmed-author:FujiiReiR,
pubmed-author:KanaiTakanoriT,
pubmed-author:KoyanagiAkemiA,
pubmed-author:MakitaShinS,
pubmed-author:NemotoYasuhiroY,
pubmed-author:OkamotoRyuichiR,
pubmed-author:OkumuraKoK,
pubmed-author:OshimaShigeruS,
pubmed-author:TotsukaTerujiT,
pubmed-author:WatanabeMamoruM,
pubmed-author:YagitaHideoH
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pubmed:issnType |
Print
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pubmed:volume |
35
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
1773-85
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:15902682-Animals,
pubmed-meshheading:15902682-Antigens, CD,
pubmed-meshheading:15902682-Antigens, Differentiation,
pubmed-meshheading:15902682-Antigens, Surface,
pubmed-meshheading:15902682-Apoptosis Regulatory Proteins,
pubmed-meshheading:15902682-CTLA-4 Antigen,
pubmed-meshheading:15902682-Chronic Disease,
pubmed-meshheading:15902682-Colitis,
pubmed-meshheading:15902682-Disease Models, Animal,
pubmed-meshheading:15902682-Female,
pubmed-meshheading:15902682-Interleukin-4,
pubmed-meshheading:15902682-Mice,
pubmed-meshheading:15902682-Mice, Inbred BALB C,
pubmed-meshheading:15902682-Programmed Cell Death 1 Receptor,
pubmed-meshheading:15902682-Receptors, Interleukin-2,
pubmed-meshheading:15902682-T-Lymphocytes, Regulatory
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pubmed:year |
2005
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pubmed:articleTitle |
Regulation of murine chronic colitis by CD4+CD25- programmed death-1+ T cells.
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pubmed:affiliation |
Department of Gastroenterology and Hepatology, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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