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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2003-1-17
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pubmed:abstractText |
Antigen-specific suppression of a previously primed immune response is a major challenge for immunotherapy of autoimmune disease. RelB activation is required for myeloid DC differentiation. Here, we show that antigen-exposed DCs in which RelB function is inhibited lack cell surface CD40, prevent priming of immunity, and suppress previously primed immune responses. DCs generated from CD40-deficient mice similarly confer suppression. Regulatory CD4+ T cells induced by the DCs transfer antigen-specific "infectious" tolerance to primed recipients in an interleukin-10-dependent fashion. Thus CD40, regulated by RelB activity, determines the consequences of antigen presentation by myeloid DCs. These observations have significance for autoimmune immunotherapy and suggest a mechanism by which peripheral tolerance might be constitutively maintained by RelB(-) CD40(-) DCs.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD40,
http://linkedlifedata.com/resource/pubmed/chemical/Hemocyanin,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Relb protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor RelB,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/keyhole-limpet hemocyanin
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1074-7613
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
18
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
155-67
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12530984-Animals,
pubmed-meshheading:12530984-Antigens,
pubmed-meshheading:12530984-Antigens, CD40,
pubmed-meshheading:12530984-Autoimmune Diseases,
pubmed-meshheading:12530984-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12530984-Dendritic Cells,
pubmed-meshheading:12530984-Hemocyanin,
pubmed-meshheading:12530984-Immune Tolerance,
pubmed-meshheading:12530984-Immunotherapy,
pubmed-meshheading:12530984-Interferon-gamma,
pubmed-meshheading:12530984-Interleukin-10,
pubmed-meshheading:12530984-Mice,
pubmed-meshheading:12530984-Mice, Inbred BALB C,
pubmed-meshheading:12530984-Mice, Inbred C57BL,
pubmed-meshheading:12530984-Mice, Knockout,
pubmed-meshheading:12530984-Ovalbumin,
pubmed-meshheading:12530984-Proto-Oncogene Proteins,
pubmed-meshheading:12530984-Transcription Factor RelB,
pubmed-meshheading:12530984-Transcription Factors
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pubmed:year |
2003
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pubmed:articleTitle |
Antigen-specific suppression of a primed immune response by dendritic cells mediated by regulatory T cells secreting interleukin-10.
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pubmed:affiliation |
Centre for Immunology and Cancer Research, University of Queensland, Princess Alexandra Hospital, Brisbane, Queensland 4102, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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