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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
1996-11-22
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pubmed:abstractText |
IL-12 stimulates both T and NK cells and is pivotal in the development of the Th1 immune response. In this work, we show that an interaction between CD2 and CD58 on activated T cells and monocytes, respectively, regulates the T cell response to IL-12. B cells provide little IL-12-specific costimulation, and this correlates with the low level of CD58 on B cells relative to monocytes and the lack of significant up-regulation in response to IFN-gamma or PHA activation. CHO cell transfectants expressing CD58 at a level comparable with that found on monocytes restore IL-12 responsiveness to APC-depleted T cells. This effect is not observed with CHO cells expressing CD48, a second CD2 ligand with a low avidity for CD2 relative to CD58. Thus, in addition to augmenting adhesion between T cells and their cognate APCs and facilitating TCR-triggered activation, the CD2-CD58 interaction uniquely optimizes the T cell response to IL-12.
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pubmed:grant |
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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/Adjuvants, Immunologic,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD2,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD58,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Phytohemagglutinins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-12
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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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 |
157
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1886-93
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8757306-Adjuvants, Immunologic,
pubmed-meshheading:8757306-Adult,
pubmed-meshheading:8757306-Animals,
pubmed-meshheading:8757306-Antibodies, Monoclonal,
pubmed-meshheading:8757306-Antigen-Presenting Cells,
pubmed-meshheading:8757306-Antigens, CD2,
pubmed-meshheading:8757306-Antigens, CD58,
pubmed-meshheading:8757306-Binding, Competitive,
pubmed-meshheading:8757306-CHO Cells,
pubmed-meshheading:8757306-Cricetinae,
pubmed-meshheading:8757306-Down-Regulation,
pubmed-meshheading:8757306-Humans,
pubmed-meshheading:8757306-Interleukin-12,
pubmed-meshheading:8757306-Interphase,
pubmed-meshheading:8757306-Lymphocyte Activation,
pubmed-meshheading:8757306-Lymphocyte Depletion,
pubmed-meshheading:8757306-Middle Aged,
pubmed-meshheading:8757306-Monocytes,
pubmed-meshheading:8757306-Phytohemagglutinins,
pubmed-meshheading:8757306-Receptors, Interleukin,
pubmed-meshheading:8757306-Receptors, Interleukin-12,
pubmed-meshheading:8757306-T-Lymphocytes,
pubmed-meshheading:8757306-Transfection
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pubmed:year |
1996
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pubmed:articleTitle |
Molecular interaction between CD58 and CD2 counter-receptors mediates the ability of monocytes to augment T cell activation by IL-12.
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pubmed:affiliation |
Laboratory of Immunobiology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
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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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