Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2002-5-30
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.
pubmed:language
eng
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)
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
99
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4509-16
pubmed:dateRevised
2011-11-17
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
pubmed:year
2002
pubmed:articleTitle
The lymphoproliferative defect in CTLA-4-deficient mice is ameliorated by an inhibitory NK cell receptor.
pubmed:affiliation
Department of Pathology, University of Massachusetts Medical School, Worcester, 01655, USA. cynthia.chambers@umassmed.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't