|
rdf:type |
|
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lifeskim:mentions |
umls-concept:C0011306,
umls-concept:C0021747,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0332307,
umls-concept:C0871261,
umls-concept:C1167395,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1415900,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1704632,
umls-concept:C1706438,
umls-concept:C1706817,
umls-concept:C1710082,
umls-concept:C2003941,
umls-concept:C2698600,
umls-concept:C2911692
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|
pubmed:issue |
10
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pubmed:dateCreated |
2011-9-28
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pubmed:abstractText |
Despite lack of tumor control in many models, spontaneous T cell priming occurs frequently in response to a growing tumor. However, the innate immune mechanisms that promote natural antitumor T cell responses are undefined. In human metastatic melanoma, there was a correlation between a type I interferon (IFN) transcriptional profile and T cell markers in metastatic tumor tissue. In mice, IFN-? was produced by CD11c(+) cells after tumor implantation, and tumor-induced T cell priming was defective in mice lacking IFN-?/?R or Stat1. IFN signaling was required in the hematopoietic compartment at the level of host antigen-presenting cells, and selectively for intratumoral accumulation of CD8?(+) dendritic cells, which were demonstrated to be essential using Batf3(-/-) mice. Thus, host type I IFNs are critical for the innate immune recognition of a growing tumor through signaling on CD8?(+) DCs.
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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 |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1540-9538
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
26
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pubmed:volume |
208
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2005-16
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pubmed:meshHeading |
pubmed-meshheading:21930765-Animals,
pubmed-meshheading:21930765-CD8-Positive T-Lymphocytes,
pubmed-meshheading:21930765-Cell Line, Tumor,
pubmed-meshheading:21930765-Dendritic Cells,
pubmed-meshheading:21930765-Humans,
pubmed-meshheading:21930765-Immunity, Innate,
pubmed-meshheading:21930765-Interferon Type I,
pubmed-meshheading:21930765-Lymph Nodes,
pubmed-meshheading:21930765-Lymphatic Metastasis,
pubmed-meshheading:21930765-Lymphocyte Subsets,
pubmed-meshheading:21930765-Melanoma,
pubmed-meshheading:21930765-Mice,
pubmed-meshheading:21930765-Mice, Inbred C57BL,
pubmed-meshheading:21930765-Mice, Knockout,
pubmed-meshheading:21930765-STAT1 Transcription Factor,
pubmed-meshheading:21930765-Signal Transduction
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pubmed:year |
2011
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pubmed:articleTitle |
Host type I IFN signals are required for antitumor CD8+ T cell responses through CD8{alpha}+ dendritic cells.
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pubmed:affiliation |
Department of Pathology and Department of Medicine, Section of Hematology/Oncology, the University of Chicago, Chicago, IL, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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