rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
12
|
pubmed:dateCreated |
2002-5-30
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pubmed:abstractText |
T-cell responses are regulated by activating and inhibiting signals. CD28 and its homologue, cytotoxic T-lymphocyte antigen 4 (CTLA-4), are the primary regulatory molecules that enhance or inhibit T-cell activation, respectively. Recently it has been shown that inhibitory natural killer (NK) cell receptors (NKRs) are expressed on subsets of T cells. It has been proposed that these receptors may also play an important role in regulating T-cell responses. However, the extent to which the NKRs modulate peripheral T-cell homeostasis and activation in vivo remains unclear. In this report we show that NK cell inhibitory receptor Ly49A engagement on T cells dramatically limits T-cell activation and the resultant lymphoproliferative disorder that occurs in CTLA-4-deficient mice. Prevention of activation and expansion of the potentially autoreactive CTLA-4(-/-) T cells by the Ly49A-mediated inhibitory signal demonstrates that NKR expression can play an important regulatory role in T-cell homeostasis in vivo. These results demonstrate the importance of inhibitory signals in T-cell homeostasis and suggest the common biochemical basis of inhibitory signaling pathways in T lymphocytes.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
|
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, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoconjugates,
http://linkedlifedata.com/resource/pubmed/chemical/Klra1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, NK Cell Lectin-Like,
http://linkedlifedata.com/resource/pubmed/chemical/abatacept,
http://linkedlifedata.com/resource/pubmed/chemical/histocompatibility antigen H-2D(b)
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
|
pubmed:issn |
0006-4971
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
|
pubmed:volume |
99
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
4509-16
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12036882-Animals,
pubmed-meshheading:12036882-Antigens, CD,
pubmed-meshheading:12036882-Antigens, Differentiation,
pubmed-meshheading:12036882-Antigens, Ly,
pubmed-meshheading:12036882-CTLA-4 Antigen,
pubmed-meshheading:12036882-Carrier Proteins,
pubmed-meshheading:12036882-H-2 Antigens,
pubmed-meshheading:12036882-Homeostasis,
pubmed-meshheading:12036882-Immunoconjugates,
pubmed-meshheading:12036882-Killer Cells, Natural,
pubmed-meshheading:12036882-Lectins, C-Type,
pubmed-meshheading:12036882-Lymphocyte Activation,
pubmed-meshheading:12036882-Lymphoproliferative Disorders,
pubmed-meshheading:12036882-Membrane Proteins,
pubmed-meshheading:12036882-Mice,
pubmed-meshheading:12036882-Mice, Knockout,
pubmed-meshheading:12036882-NK Cell Lectin-Like Receptor Subfamily A,
pubmed-meshheading:12036882-Receptors, Immunologic,
pubmed-meshheading:12036882-Receptors, NK Cell Lectin-Like,
pubmed-meshheading:12036882-Signal Transduction,
pubmed-meshheading:12036882-T-Lymphocytes
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pubmed:year |
2002
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pubmed:articleTitle |
The lymphoproliferative defect in CTLA-4-deficient mice is ameliorated by an inhibitory NK cell receptor.
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pubmed:affiliation |
Department of Pathology, University of Massachusetts Medical School, Worcester, 01655, USA. cynthia.chambers@umassmed.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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