Evidence map›Paper›PMID 25111504›Full record

ArticlePloS one2014

Inhibition of breast cancer resistance protein (ABCG2) in human myeloid dendritic cells induces potent tolerogenic functions during LPS stimulation.

Jun-O Jin, Wei Zhang, Ka-Wing Wong, Minseok Kwak, Ian R van Driel, Qing Yu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Impact ofGenes · 2021
    Article
  3. Article
  4. Alarmins and Antitumor Immunity.Clinical therapeutics · 2016
    Review
  5. Article
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

6 authors at 3 institutions in 3 countries.

Jun-O JinShanghai Public Health Clinical Center, Shanghai Medical College, Fudan University, Shanghai, China.
Wei ZhangShanghai Public Health Clinical Center, Shanghai Medical College, Fudan University, Shanghai, China.
Ka-Wing WongShanghai Public Health Clinical Center, Shanghai Medical College, Fudan University, Shanghai, China.
Minseok KwakDepartment of Chemistry, Pukyong National University, Busan, South Korea.
Ian R van DrielDepartment of Biochemistry and Molecular Biology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Victoria, Australia.
Qing YuDepartment of Immunology and Infectious Diseases, The Forsyth Institute, Cambridge, Massachusetts, United States of America.
Shanghai Public Health Clinical Center · CNPukyong National University · KRUniversity of Melbourne · AU

Funding

Regulation and Function of Interleukin-7 in Primary Sjogrens SyndromeR01DE023838 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI YU, QING · 2014 to 2018
$2.4M
Mechanisms and Therapeutic Modulation of T Cell Autoimmune Responses in Sjogren's SyndromeR56DE023838 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI CHA, SEUNGHEE, YU, QING · 2020 to 2020
$532k
NIDCR NIH HHS R01 DE023838NIDCR NIH HHS R56 DE023838
6 · The paper itself

Abstract

Breast cancer resistance protein (ABCG2), a member of the ATP-binding cassette transporters has been identified as a major determinant of multidrug resistance (MDR) in cancer cells, but ABC transporter inhibition has limited therapeutic value in vivo. In this research, we demonstrated that inhibition of efflux transporters ABCG2 induced the generation of tolerogenic DCs from human peripheral blood myeloid DCs (mDCs). ABCG2 expression was present in mDCs and was further increased by LPS stimulation. Treatment of CD1c+ mDCs with an ABCG2 inhibitor, Ko143, during LPS stimulation caused increased production of IL-10 and decreased production of pro-inflammatory cytokines and decreased expression of CD83 and CD86. Moreover, inhibition of ABCG2 in monocyte-derived DCs (MDDCs) abrogated the up-regulation of co-stimulatory molecules and production of pro-inflammatory cytokines in these cells in response to LPS. Furthermore, CD1c+ mDCs stimulated with LPS plus Ko143 inhibited the proliferation of allogeneic and superantigen-specific syngenic CD4+ T cells and promoted expansion of CD25+FOXP3+ regulatory T (Treg) cells in an IL-10-dependent fashion. These tolerogenic effects of ABCG2 inhibition could be abolished by ERK inhibition. Thus, we demonstrated that inhibition of ABCG2 in LPS-stimulated mDCs can potently induce tolerogenic potentials in these cells, providing crucial new information that could lead to development of better strategies to combat MDR cancer.

Indexed as

AdenosineATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Dendritic CellsDiketopiperazinesExtracellular Signal-Regulated MAP KinasesGene Knockdown TechniquesHeterocyclic Compounds, 4 or More RingsHumansInterleukin-10LipopolysaccharidesMyeloid CellsNeoplasm ProteinsPhosphorylationT-Lymphocytes, RegulatoryUp-Regulation3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl esterABCG2 protein, humanAdenosineATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2DiketopiperazinesExtracellular Signal-Regulated MAP KinasesHeterocyclic Compounds, 4 or More RingsInterleukin-10LipopolysaccharidesNeoplasm Proteins

Identifiers

PMID25111504
PMCPMC4128747
OpenAlexW1981311440

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.