rdf:type |
|
lifeskim:mentions |
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0022688,
umls-concept:C0039194,
umls-concept:C0425152,
umls-concept:C0439064,
umls-concept:C0597357,
umls-concept:C0678226,
umls-concept:C1334309,
umls-concept:C1337103,
umls-concept:C1511559,
umls-concept:C1705388
|
pubmed:issue |
5
|
pubmed:dateCreated |
2001-3-14
|
pubmed:abstractText |
Inhibitory receptors specific for MHC class I molecules are expressed on partially overlapping subpopulations of NK cells and memory T cells. A central question pertinent to NK cell development and function is how the combinatorial expression of different receptors with distinct class I specificities affects functional recognition. We therefore studied the quantitative effects resulting from class I engagement of multiple inhibitory Ly49 receptors. We used a transgenic mouse model in which all NK cells and T cells express two different Ly49 receptors with shared class I specificity. Comparisons of cells from these mice with cells from single transgenic mice and wild-type mice revealed that Ly49 receptors cumulatively inhibit lymphocyte effector functions. Multiple Ly49 interactions also had a cumulative impact on NK cell development. The findings suggest that the interactions of inhibitory receptors with class I are interpreted quantitatively rather than as on/off switches. They have intriguing implications concerning NK cell tolerance and reactivity toward cells with extinguished expression of a limited number of class I molecules.
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pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Ly,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/H-2K(K) antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
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/histocompatibility antigen H-2D(b)
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
|
pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
166
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
3002-7
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:11207249-Animals,
pubmed-meshheading:11207249-Antigens, Ly,
pubmed-meshheading:11207249-Carrier Proteins,
pubmed-meshheading:11207249-Cells, Cultured,
pubmed-meshheading:11207249-Cytotoxicity, Immunologic,
pubmed-meshheading:11207249-H-2 Antigens,
pubmed-meshheading:11207249-Immune Tolerance,
pubmed-meshheading:11207249-Killer Cells, Lymphokine-Activated,
pubmed-meshheading:11207249-Killer Cells, Natural,
pubmed-meshheading:11207249-Lectins, C-Type,
pubmed-meshheading:11207249-Lymphocyte Activation,
pubmed-meshheading:11207249-Lymphocyte Culture Test, Mixed,
pubmed-meshheading:11207249-Membrane Glycoproteins,
pubmed-meshheading:11207249-Membrane Proteins,
pubmed-meshheading:11207249-Mice,
pubmed-meshheading:11207249-Mice, Inbred C57BL,
pubmed-meshheading:11207249-Mice, Inbred DBA,
pubmed-meshheading:11207249-Mice, Transgenic,
pubmed-meshheading:11207249-Receptors, Immunologic,
pubmed-meshheading:11207249-Receptors, NK Cell Lectin-Like,
pubmed-meshheading:11207249-T-Lymphocytes,
pubmed-meshheading:11207249-Tumor Cells, Cultured,
pubmed-meshheading:11207249-Wasting Syndrome
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pubmed:year |
2001
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pubmed:articleTitle |
Cumulative inhibition of NK cells and T cells resulting from engagement of multiple inhibitory Ly49 receptors.
|
pubmed:affiliation |
Institute for Virology and Immunobiology, University of Wurzburg, Wurzburg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|