Evidence map›Paper›PMID 22622800›Full record

ArticleEuropean journal of immunology2012

IL-10 deficiency blocks the ability of LPS to regulate expression of tolerance-related molecules on dendritic cells.

Fang Zhou, Bogoljub Ciric, Hongmei Li, Yaping Yan, Ke Li, Melissa Cullimore, Elisabetta Lauretti, Patricia Gonnella, Guang-Xian Zhang, Abdolmohamad Rostami

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
  3. Manifestation of lipopolysaccharide-induced tolerance in neuro-glial primary cultures of the rat afferent somatosensory system.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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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

10 authors at 1 institution in 1 country.

Fang ZhouDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Bogoljub Ciric
Hongmei Li
Yaping Yan
Ke Li
Melissa Cullimore
Elisabetta Lauretti
Patricia Gonnella
Guang-Xian Zhang
Abdolmohamad Rostami
Thomas Jefferson University · US

Funding

The Role of Dendritic Cells in Intravenous ToleranceR01NS048435 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2004 to 2013
$2.9M
The Role of the TH17 cells in the pathogenesis of EAER01NS046782 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ROSTAMI, A.M. · 2003 to 2013
$2.7M
NINDS NIH HHS R01 NS046782NINDS NIH HHS R01 NS048435NINDS NIH HHS R01NS048435
6 · The paper itself

Abstract

Interleukin-10 (IL-10) is an anti-inflammatory cytokine that plays an important role in regulating the local inflammatory immune response, but regulatory mechanisms of this cytokine have not been fully elucidated. Here, we demonstrate that IL-10 deficiency renders LPS treatment ineffective in regulating the expression of CD40, CD80, CD86, B7-H2, and B7-DC on dendritic cells (DCs) and blocks upregulation of IL-27. This inability to respond to LPS was found in both IL-10(-/-) bone marrow derived and splenic DCs. Compared with wild-type DCs, IL-10(-/-) DCs expressed similar levels of TLR4 and CD14, but produced less LPS-binding protein. The deficiency in LPS-binding protein production may explain the failure of IL-10(-/-) DCs to respond normally to LPS. Moreover, lack of IL-10 modulated the proportions of CD11c(+) CD8(+) and CD11c(+) B220(+) DCs, which play an important role in local inflammatory responses and tolerance. IL-10 deficiency also blocked expression of galectin-1, CD205, and CD103, which are necessary for central and peripheral tolerance. While they did not respond to LPS, IL-10(-/-) DCs produced increased levels of IL-6 and CCL4 after TNF-α treatment. Together, our results demonstrate that IL-10 deficiency affects the immune functions of DCs, which may contribute to the increased severity of autoimmune diseases seen in IL-10(-/-) mice.

Indexed as

Acute-Phase ProteinsAnimalsAntigens, CDCarrier ProteinsCell DifferentiationChemokine CCL4Dendritic CellsFemaleGalectin 1Histocompatibility Antigens Class IIIntegrin alpha ChainsInterleukin-10Interleukin-6InterleukinsLectins, C-TypeLipopolysaccharide-Binding ProteinAcute-Phase Proteinsalpha E integrinsAntigens, CDCarrier ProteinsChemokine CCL4CPG-oligonucleotideDEC-205 receptorGalectin 1Histocompatibility Antigens Class IIIl27 protein, mouseIntegrin alpha ChainsInterleukin-10Interleukin-6InterleukinsLectins, C-TypeLipopolysaccharide-Binding ProteinLipopolysaccharidesMembrane GlycoproteinsMinor Histocompatibility AntigensOligodeoxyribonucleotidesReceptors, Cell Surface

Identifiers

PMID22622800
PMCPMC3596886
OpenAlexW1514327587

What OpenQuestion holds

Textmetadata
LicenceTDM
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.