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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2001-11-20
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pubmed:abstractText |
Eosinophils in tissues are often present in intimate contact with T cells in allergic and parasitic diseases. Resting eosinophils do not express MHC class II proteins or costimulatory B7 molecules and fail to induce proliferation of T cells to Ags. IL-5 and GM-CSF induce MHC class II and B7 expression on eosinophils and have been reported in some studies to induce eosinophils to present Ag to T cells. The cytokine IL-3, like IL-5 and GM-CSF, is a survival and activating factor for eosinophils and the IL-3 receptor shares with the IL-5 and GM-CSF receptors a common signal transducing beta-chain. IL-3-treated eosinophils expressed HLA-DR and B7.2, but not B7.1 on their surface and supported T cell proliferation in response to the superantigen toxic shock syndrome toxin 1, as well as the proliferation of HLA-DR-restricted tetanus toxoid (TT) and influenza hemagglutinin-specific T cell clones to antigenic peptides. This was inhibited by anti-B7.2 mAb. In contrast, IL-3-treated eosinophils were unable to present native TT Ag to either resting or TT-specific cloned T cells. In parallel experiments, eosinophils treated with IL-5 or GM-CSF were also found to present superantigen and antigenic peptides, but not native Ag, to T cells. These results suggest that eosinophils are deficient in Ag processing and that this deficiency is not overcome by cytokines that signal via the beta-chain. Nevertheless, our findings suggest that eosinophils activated by IL-3 may contribute to T cell activation in allergic and parasitic diseases by presenting superantigens and peptides to T cells.
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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/Antigens, Bacterial,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/CD86 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Granulocyte-Macrophage...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-3,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-5,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphokines,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Superantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Tetanus Toxoid,
http://linkedlifedata.com/resource/pubmed/chemical/eosinophil stimulating promoter
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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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 |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6097-104
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11714768-Antigen-Presenting Cells,
pubmed-meshheading:11714768-Antigens, Bacterial,
pubmed-meshheading:11714768-Antigens, CD,
pubmed-meshheading:11714768-Antigens, CD86,
pubmed-meshheading:11714768-Cell Communication,
pubmed-meshheading:11714768-Clone Cells,
pubmed-meshheading:11714768-Dose-Response Relationship, Immunologic,
pubmed-meshheading:11714768-Eosinophils,
pubmed-meshheading:11714768-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:11714768-Humans,
pubmed-meshheading:11714768-Interleukin-3,
pubmed-meshheading:11714768-Interleukin-5,
pubmed-meshheading:11714768-Lymphocyte Activation,
pubmed-meshheading:11714768-Lymphokines,
pubmed-meshheading:11714768-Membrane Glycoproteins,
pubmed-meshheading:11714768-Peptides,
pubmed-meshheading:11714768-Signal Transduction,
pubmed-meshheading:11714768-Superantigens,
pubmed-meshheading:11714768-T-Lymphocytes,
pubmed-meshheading:11714768-Tetanus Toxoid
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pubmed:year |
2001
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pubmed:articleTitle |
IL-3 induces B7.2 (CD86) expression and costimulatory activity in human eosinophils.
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pubmed:affiliation |
Division of Immunology and Department of Pediatrics, Children's Hospital, Harvard Medical School, 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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