Evidence map›Paper›PMID 28719617›Full record

ArticlePloS one2017

MicroRNA 155-deficiency leads to decreased autoantibody levels and reduced severity of nephritis and pneumonitis in pristane-induced lupus.

Harald Leiss, Wilhelm Salzberger, Barbara Jacobs, Irina Gessl, Nicolas Kozakowski, Stephan Blüml, Antonia Puchner, Attila Kiss, Bruno K Podesser, Josef S Smolen and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Non-Coding RNAs in CD4Frontiers in immunology · 2020
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  18. Article
  19. Antioxidant and Antisenescence Effects of Bergamot Juice.Oxidative medicine and cellular longevity · 2018
    Article
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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

11 authors at 1 institution in 1 country.

Harald LeissDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0002-5810-2240
Wilhelm SalzbergerDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Barbara JacobsDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Irina GesslDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Nicolas KozakowskiDepartment of Pathology Medical University of Vienna, Vienna, Austria.
Stephan BlümlDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Antonia PuchnerDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Attila KissCenter for Biomedical Research, Medical University of Vienna, Vienna, Austria.
Bruno K PodesserCenter for Biomedical Research, Medical University of Vienna, Vienna, Austria.
Josef S SmolenDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Georg H StummvollDepartment of Rheumatology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe herein examine the role of endogenous miR155 in the development of systemic manifestations in pristane induced lupus. MATERIALS AND

methodsSystemic lupus in miR155-deficient and wild type mice was induced upon injection of pristane and analyzed after 8 months, PBS-injected mice served as controls. Glomerulonephritis and pneumonitis were quantified using the kidney biopsy score and a newly adapted histomorphometric image analysis system; lung tissue was further analyzed by tissue cytometry. Serum levels of anti-dsDNA, anti-histone and anti-chromatin antibodies were measured by ELISA. Frequencies of B cells, activated and regulatory CD4+ T cells as well as Th1, Th2, Th17 cells were measured by flow cytometry. RT-qPCR was used to measure expression levels of interferon-signature and T-cell subset related as well as miR155-associated genes.

resultsAfter induction of lupus, miR155-deficient mice had significant less pulmonary involvement (perivascular inflammatory area in mm2/mm2 lung area 0.00092±0.00015 vs. 0.0027±0.00075, p = 0.0347) and renal disease (glomerular activity score 1.95±0.19 vs 3±0.26, p = 0.0029) compared to wild types. MiR155-deficient mice had significantly lower serum levels of disease-associated auto-antibodies and decreased frequencies of activated CD4+CD25+ (Foxp3-) cells. Upon restimulation, CD4+ cells showed a less pronounced Th2 and Th17 and a slightly decreased Th1 response in mir155-deficient mice. Pristane-treated wild types showed significantly up-regulated expression of genes related to the INF-signature (MX1, IP10, IRF7, ISG15).

conclusionsMiR155-deficient mice had less severe organ involvement, lower serum auto-antibody levels, a less prominent T cell response and lower expressions of genes jointly responsible for disease development. Thus, antagonizing miR155 might be a future approach in treating SLE.

Indexed as

AnimalsAutoantibodiesGene Expression RegulationInterferonsKidneyLungLupus Erythematosus, SystemicMiceMicroRNAsNephritisPneumoniaTerpenesT-Lymphocyte SubsetsAutoantibodiesInterferonsMicroRNAsMirn155 microRNA, mousepristaneTerpenes

Identifiers

PMID28719617
PMCPMC5515414
OpenAlexW2737017044

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Registered trials

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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.