rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0020846,
umls-concept:C0021758,
umls-concept:C0030685,
umls-concept:C0086418,
umls-concept:C0162825,
umls-concept:C0205147,
umls-concept:C0205263,
umls-concept:C0214743,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1291802,
umls-concept:C1704675,
umls-concept:C1963578
|
pubmed:issue |
2
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pubmed:dateCreated |
2000-2-10
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pubmed:abstractText |
HIV-1 glycoprotein (gp) 120 from different clades is a potent stimulus for IL-4 and IL-13 release from basophils purified from healthy individuals seronegative for Abs to HIV-1 and HIV-2. IL-4 mRNA, constitutively present in basophils, was increased after stimulation by gp120 and was inhibited cyclosporin A and tacrolimus. IL-4 and IL-13 secretion from basophils activated by gp120 was not correlated. There was a correlation between the maximum gp120- and anti-IgE-induced IL-4 release from basophils. The average t1/2 gp120-induced IL-4 release was lower than for IL-13 release. Basophils from which IgE had been dissociated by brief exposure to lactic acid no longer released IL-4 in response to gp120 or to anti-IgE. The response to a mAb cross-linking the alpha-chain of high-affinity receptor for IgE (Fc epsilon RI) was unaffected by this treatment. Three human VH3+ monoclonal IgM inhibited gp120-induced secretion of IL-4 from basophils. In contrast, VH6+ monoclonal IgM did not inhibit the release of IL-4 induced by gp120. Synthetic peptides distant from the NH2 and COOH termini of gp120MN inhibited the activating property of gp120MN. These results indicate that gp120, which acts as a viral superantigen, interacts with the VH3 region of IgE to induce the release of IL-4 and IL-13 from human Fc epsilon RI+ cells.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Envelope Protein gp120,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Heavy Chains,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Variable Region,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Myeloma Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, IgE,
http://linkedlifedata.com/resource/pubmed/chemical/Tacrolimus
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
164
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
589-95
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10623799-Adult,
pubmed-meshheading:10623799-Basophils,
pubmed-meshheading:10623799-Cyclosporine,
pubmed-meshheading:10623799-HIV Envelope Protein gp120,
pubmed-meshheading:10623799-HIV-1,
pubmed-meshheading:10623799-Humans,
pubmed-meshheading:10623799-Hydrogen-Ion Concentration,
pubmed-meshheading:10623799-Immunoglobulin E,
pubmed-meshheading:10623799-Immunoglobulin Heavy Chains,
pubmed-meshheading:10623799-Immunoglobulin M,
pubmed-meshheading:10623799-Immunoglobulin Variable Region,
pubmed-meshheading:10623799-Interleukin-13,
pubmed-meshheading:10623799-Interleukin-4,
pubmed-meshheading:10623799-Kinetics,
pubmed-meshheading:10623799-Mast Cells,
pubmed-meshheading:10623799-Middle Aged,
pubmed-meshheading:10623799-Myeloma Proteins,
pubmed-meshheading:10623799-Peptide Fragments,
pubmed-meshheading:10623799-Receptors, IgE,
pubmed-meshheading:10623799-Tacrolimus
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pubmed:year |
2000
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pubmed:articleTitle |
HIV-1 gp120 induces IL-4 and IL-13 release from human Fc epsilon RI+ cells through interaction with the VH3 region of IgE.
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pubmed:affiliation |
University of Naples Federico II, Division of Clinical Immunology and Allergy, Naples, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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