Evidence map›Paper›PMID 18259609›Full record

ArticleThe Journal of clinical investigation2008

Plasmacytoid dendritic cells induce NK cell-dependent, tumor antigen-specific T cell cross-priming and tumor regression in mice.

Chengwen Liu, Yanyan Lou, Gregory Lizée, Hong Qin, Shujuan Liu, Brian Rabinovich, Grace J Kim, Yi-Hong Wang, Yang Ye, Andrew G Sikora and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed
8.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

163 citing papers in PubMed, 303 citations in OpenAlex.

  1. Trial
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  10. CD4Cancer medicine · 2025
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  19. Human CD34Cellular and molecular life sciences : CMLS · 2023
    Article
  20. Article

103 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Chengwen LiuDepartment of Melanoma Medical Oncology, Center for Cancer Immunology Research, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Yanyan Lou
Gregory Lizée
Hong Qin
Shujuan Liu
Brian Rabinovich
Grace J Kim
Yi-Hong Wang
Yang Ye
Andrew G Sikora
Willem W Overwijk
Yong-Jun Liu
Gang Wang
Patrick Hwu
The University of Texas MD Anderson Cancer Center · USMelanoma Institute Australia · AUUnited States Food and Drug Administration · US

Funding

Plasmacytoid DC Interactions in the Generation of an Antitumor Immune ResponseR01CA123182 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI HWU, PATRICK · 2006 to 2010
$1.3M
NCI NIH HHS R01 CA123182NCI NIH HHS R01 CA123182-02
6 · The paper itself

Abstract

A prerequisite for strong adaptive antiviral immunity is the robust initial activation of the innate immune system, which is frequently mediated by TLR-activated plasmacytoid DCs (pDCs). Natural antitumor immunity is often comparatively weak, potentially due to the lack of TLR-mediated activation signals within the tumor microenvironment. To assess whether pDCs are capable of directly facilitating effective antitumor immune responses, mice bearing established subcutaneous B16 melanoma tumors were administered TLR9-activated pDCs directly into the tumor. We found that TLR9-activated pDCs induced robust, spontaneous CTL cross-priming against multiple B16 tumor antigens, leading to the regression of both treated tumors and untreated tumors at distant contralateral sites. This T cell cross-priming was mediated by conventional DCs (cDCs) and was completely dependent upon the early recruitment and activation of NK cells at the tumor site. NK cell recruitment was mediated by CCR5 via chemokines secreted by pDCs, and optimal IFN-gamma production by NK cells was mediated by OX40L expressed by pDCs. Our data thus demonstrated that activated pDCs are capable of initiating effective and systemic antitumor immunity through the orchestration of an immune cascade involving the sequential activation of NK cells, cDCs, and CD8(+) T cells.

Indexed as

AnimalsAntigens, NeoplasmCytokinesDendritic CellsFemaleInterferon-gammaKiller Cells, NaturalMelanoma, ExperimentalMembrane GlycoproteinsMiceMice, Inbred C57BLOligodeoxyribonucleotidesOX40 LigandReceptors, CCR5Receptors, OX40T-LymphocytesAntigens, NeoplasmCPG-oligonucleotideCytokinesInterferon-gammaMembrane GlycoproteinsOligodeoxyribonucleotidesOX40 LigandReceptors, CCR5Receptors, OX40Tlr9 protein, mouseTnfrsf4 protein, mouseTnfsf4 protein, mouseToll-Like Receptor 9Tumor Necrosis Factors

Identifiers

PMID18259609
PMCPMC2230660
OpenAlexW2039248453

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.