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rdf:type |
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lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0021747,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0220905,
umls-concept:C0332307,
umls-concept:C0851285,
umls-concept:C0871261,
umls-concept:C1332714,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1415900,
umls-concept:C1704632,
umls-concept:C1706438,
umls-concept:C1706817,
umls-concept:C2698600,
umls-concept:C2911692
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pubmed:issue |
1
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pubmed:dateCreated |
2004-12-21
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pubmed:abstractText |
Pleiotropic, immunomodulatory effects of type I IFN on T cell responses are emerging. We used vaccine-induced, antiviral CD8(+) T cell responses in IFN-beta (IFN-beta(-/-))- or type I IFN receptor (IFNAR(-/-))-deficient mice to study immunomodulating effects of type I IFN that are not complicated by the interference of a concomitant virus infection. Compared with normal B6 mice, IFNAR(-/-) or IFN-beta(-/-) mice have normal numbers of CD4(+) and CD8(+) T cells, and CD25(+)FoxP3(+) T regulatory (T(R)) cells in liver and spleen. Twice as many CD8(+) T cells specific for different class I-restricted epitopes develop in IFNAR(-/-) or IFN-beta(-/-) mice than in normal animals after peptide- or DNA-based vaccination. IFN-gamma and TNF-alpha production and clonal expansion of specific CD8(+) T cells from normal and knockout mice are similar. CD25(+)FoxP3(+) T(R) cells down-modulate vaccine-primed CD8(+) T cell responses in normal, IFNAR(-/-), or IFN-beta(-/-) mice to a comparable extent. Low IFN-alpha or IFN-beta doses (500-10(3) U/mouse) down-modulate CD8(+) T cells priming in vivo. IFNAR- and IFN-beta-deficient mice generate 2- to 3-fold lower numbers of IL-10-producing CD4(+) T cells after polyclonal or specific stimulation in vitro or in vivo. CD8(+) T cell responses are thus subjected to negative control by both CD25(+)FoxP3(+) T(R) cells and CD4(+)IL-10(+) T(R1) cells, but only development of the latter T(R) cells depends on type I IFN.
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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/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Foxp3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interferon,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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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 |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
99-109
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15611232-Adoptive Transfer,
pubmed-meshheading:15611232-Animals,
pubmed-meshheading:15611232-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15611232-DNA-Binding Proteins,
pubmed-meshheading:15611232-Dendritic Cells,
pubmed-meshheading:15611232-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:15611232-Forkhead Transcription Factors,
pubmed-meshheading:15611232-Interferon Type I,
pubmed-meshheading:15611232-Interferon-gamma,
pubmed-meshheading:15611232-Interleukin-10,
pubmed-meshheading:15611232-Liver,
pubmed-meshheading:15611232-Lymphocyte Activation,
pubmed-meshheading:15611232-Mice,
pubmed-meshheading:15611232-Mice, Knockout,
pubmed-meshheading:15611232-Receptors, Interferon,
pubmed-meshheading:15611232-Receptors, Interleukin-2,
pubmed-meshheading:15611232-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15611232-Spleen,
pubmed-meshheading:15611232-Th1 Cells,
pubmed-meshheading:15611232-Tumor Necrosis Factor-alpha
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pubmed:year |
2005
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pubmed:articleTitle |
Type I IFN negatively regulates CD8+ T cell responses through IL-10-producing CD4+ T regulatory 1 cells.
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pubmed:affiliation |
Department of Medical Microbiology and Immunology, University of Ulm, Helmholtzstrasse 8/1, D-89081 Ulm, Germany. nektarios.dikopoulos@medizin.uni-ulm.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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