Evidence map›Paper›PMID 27509492›Full record

ArticleInternational journal of molecular sciences2016

MicroRNA-155 Mediates Augmented CD40 Expression in Bone Marrow Derived Plasmacytoid Dendritic Cells in Symptomatic Lupus-Prone NZB/W F1 Mice.

Sheng Yan, Lok Yan Yim, Rachel Chun Yee Tam, Albert Chan, Liwei Lu, Chak Sing Lau, Vera Sau-Fong Chan

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. miR-155: An Important Role in Inflammation Response.Journal of immunology research · 2022
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. The CD40-ATP-P2XFrontiers in immunology · 2019
    Review
  8. MicroRNAs in Autoimmunity and Hematological Malignancies.International journal of molecular sciences · 2018
    Review
  9. Review
  10. Article
  11. Review
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

7 authors at 1 institution in 1 country.

Sheng YanDepartments of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. ssyan@hku.hk.
Lok Yan YimDepartments of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. adayim@connect.hku.hk.
Rachel Chun Yee TamDepartments of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. rach0806@connect.hku.hk.
Albert ChanDepartments of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. wkchanf@hku.hk.
Liwei LuDepartments of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. liweilu@hkucc.hku.hk.
Chak Sing LauDepartments of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. sfvchan@hku.hk.
Vera Sau-Fong ChanDepartments of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China. cslau@hku.hk.
Chinese University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic multi-organ autoimmune disease characterized by hyperactivated immune responses to self-antigens and persistent systemic inflammation. Previously, we reported abnormalities in circulating and bone marrow (BM)-derived plasmacytoid dendritic cells (pDCs) from SLE patients. Here, we aim to seek for potential regulators that mediate functional aberrations of pDCs in SLE. BM-derived pDCs from NZB/W F1 mice before and after the disease onset were compared for toll-like receptor (TLR) induced responses and microRNA profile changes. While pDCs derived from symptomatic mice were phenotypically comparable to pre-symptomatic ones, functionally they exhibited hypersensitivity to TLR7 but not TLR9 stimulation, as represented by the elevated upregulation of CD40, CD86 and MHC class II molecules upon R837 stimulation. Upregulated induction of miR-155 in symptomatic pDCs following TLR7 stimulation was observed. Transfection of miR-155 mimics in pre-symptomatic pDCs induced an augmented expression of Cd40, which is consistent with the increased CD40 expression in symptomatic pDCs. Overall, our results provide evidence for miR-155-mediated regulation in pDC functional abnormalities in SLE. Findings from this study contribute to a better understanding of SLE pathogenesis and ignite future interests in evaluating the molecular regulation in autoimmunity.

Indexed as

AnimalsAntigen PresentationBone Marrow CellsCD40 AntigensCells, CulturedDendritic CellsFemaleGene ExpressionLupus Erythematosus, SystemicMembrane GlycoproteinsMice, TransgenicMicroRNAsRNA InterferenceToll-Like Receptor 7CD40 AntigensMembrane GlycoproteinsMicroRNAsMirn155 microRNA, mouseTlr7 protein, mouseToll-Like Receptor 7microRNAsplasmacytoid dendritic cellssystemic lupus erythematosustoll-like receptor 7

Identifiers

PMID27509492
PMCPMC5000679
OpenAlexW2497860864

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.