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rdf:type |
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lifeskim:mentions |
umls-concept:C0003320,
umls-concept:C0011306,
umls-concept:C0023395,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0205228,
umls-concept:C0333668,
umls-concept:C1332717,
umls-concept:C1334145,
umls-concept:C1413244,
umls-concept:C1515655,
umls-concept:C1706438,
umls-concept:C2698600
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pubmed:issue |
2
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pubmed:dateCreated |
2002-8-28
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pubmed:abstractText |
Cytotoxic T lymphocytes (CTL) respond to antigenic peptides presented on MHC class I molecules. On most cells, these peptides are exclusively of endogenous, cytosolic origin. Bone marrow-derived antigen-presenting cells, however, harbor a unique pathway for MHC I presentation of exogenous antigens. This mechanism permits cross-presentation of pathogen-infected cells and the priming of CTL responses against intracellular microbial infections. Here, we report a novel diphtheria toxin-based system that allows the inducible, short-term ablation of dendritic cells (DC) in vivo. We show that in vivo DC are required to cross-prime CTL precursors. Our results thus define a unique in vivo role of DC, i.e., the sensitization of the immune system for cell-associated antigens. DC-depleted mice fail to mount CTL responses to infection with the intracellular bacterium Listeria monocytogenes and the rodent malaria parasite Plasmodium yoelii.
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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 |
Aug
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pubmed:issn |
1074-7613
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pubmed:author |
pubmed-author:De los SantosKeniaK,
pubmed-author:JungSteffenS,
pubmed-author:KoKyungK,
pubmed-author:LangRichard ARA,
pubmed-author:LittmanDan RDR,
pubmed-author:PamerEric GEG,
pubmed-author:SanoGen-IchiroG,
pubmed-author:SparwasserTimT,
pubmed-author:UnutmazDeryaD,
pubmed-author:VuthooriSriS,
pubmed-author:WongPhillipP,
pubmed-author:WuShengjiS,
pubmed-author:ZavalaFidelF
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pubmed:issnType |
Print
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
211-20
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pubmed:dateRevised |
2011-1-25
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pubmed:meshHeading |
pubmed-meshheading:12196292-Animals,
pubmed-meshheading:12196292-CD8-Positive T-Lymphocytes,
pubmed-meshheading:12196292-Dendritic Cells,
pubmed-meshheading:12196292-Diphtheria Toxin,
pubmed-meshheading:12196292-Integrin alphaXbeta2,
pubmed-meshheading:12196292-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:12196292-Listeria monocytogenes,
pubmed-meshheading:12196292-Liver,
pubmed-meshheading:12196292-Mice,
pubmed-meshheading:12196292-Mice, Inbred BALB C,
pubmed-meshheading:12196292-Mice, Inbred C57BL,
pubmed-meshheading:12196292-Mice, Transgenic,
pubmed-meshheading:12196292-Models, Animal,
pubmed-meshheading:12196292-Plasmodium yoelii,
pubmed-meshheading:12196292-Receptors, Cell Surface,
pubmed-meshheading:12196292-Recombinant Fusion Proteins,
pubmed-meshheading:12196292-T-Lymphocytes, Cytotoxic
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pubmed:year |
2002
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pubmed:articleTitle |
In vivo depletion of CD11c+ dendritic cells abrogates priming of CD8+ T cells by exogenous cell-associated antigens.
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pubmed:affiliation |
Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York 10016, USA. s.jung@weizmann.ac.il
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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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