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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2002-1-21
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pubmed:abstractText |
Specific and selective immunological unresponsiveness to donor alloantigens can be induced in vivo. We have shown previously that CD25+CD4+ T cells from mice exhibiting long-term operational tolerance to donor alloantigens can regulate rejection of allogeneic skin grafts mediated by CD45RB(high)CD4+ T cells. In this study, we wished to determine whether donor-specific regulatory cells can be generated during the induction phase of unresponsiveness, i.e., before transplantation. We provide evidence that pretreatment with anti-CD4 Ab plus a donor-specific transfusion generates donor-specific regulatory CD25+CD4+ T cells that can suppress rejection of skin grafts mediated by naive CD45RB(high)CD4+ T cells. Regulatory cells were contained only in the CD25+ fraction, as equivalent numbers of CD25-CD4+ T cells were unable to regulate rejection. This pretreatment strategy led to increased expression of CD122 by the CD25+CD4+ T cells. Blockade of both the IL-10 and CTLA-4 pathways abrogated immunoregulation mediated by CD25+ T cells, suggesting that IL-10 and CTLA-4 are required for the functional activity of this population of immunoregulatory T cells. In clinical transplantation, the generation of regulatory T cells that could provide dynamic control of rejection responses is a possible route to permanent graft survival without the need for long-term immunosuppression.
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Isoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/abatacept
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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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 |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1080-6
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11801641-Animals,
pubmed-meshheading:11801641-Antibodies, Monoclonal,
pubmed-meshheading:11801641-Antigens, CD,
pubmed-meshheading:11801641-Antigens, CD4,
pubmed-meshheading:11801641-Antigens, Differentiation,
pubmed-meshheading:11801641-Blood Transfusion,
pubmed-meshheading:11801641-CD4-Positive T-Lymphocytes,
pubmed-meshheading:11801641-CTLA-4 Antigen,
pubmed-meshheading:11801641-Epitopes, T-Lymphocyte,
pubmed-meshheading:11801641-Graft Rejection,
pubmed-meshheading:11801641-Immunoconjugates,
pubmed-meshheading:11801641-Interleukin-10,
pubmed-meshheading:11801641-Isoantigens,
pubmed-meshheading:11801641-Lymphocyte Activation,
pubmed-meshheading:11801641-Mice,
pubmed-meshheading:11801641-Mice, Inbred BALB C,
pubmed-meshheading:11801641-Mice, Inbred C57BL,
pubmed-meshheading:11801641-Mice, Inbred CBA,
pubmed-meshheading:11801641-Mice, Knockout,
pubmed-meshheading:11801641-Receptors, Interleukin-2,
pubmed-meshheading:11801641-T-Lymphocyte Subsets,
pubmed-meshheading:11801641-Transplantation Conditioning,
pubmed-meshheading:11801641-Transplantation Tolerance
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pubmed:year |
2002
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pubmed:articleTitle |
CD25+CD4+ regulatory T cells prevent graft rejection: CTLA-4- and IL-10-dependent immunoregulation of alloresponses.
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pubmed:affiliation |
Nuffield Department of Surgery, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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