Evidence map›Paper›PMID 23949802›Full record

ArticleJournal of the American Society of Nephrology : JASN2013

MicroRNA-155 drives TH17 immune response and tissue injury in experimental crescentic GN.

Christian F Krebs, Sonja Kapffer, Hans-Joachim Paust, Tilman Schmidt, Sabrina B Bennstein, Anett Peters, Gesa Stege, Silke R Brix, Catherine Meyer-Schwesinger, Roman-Ulrich Müller and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. MicroRNAs in atopic dermatitis: A systematic review.Journal of cellular and molecular medicine · 2020
    Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Post-transcriptional checkpoints in autoimmunity.Nature reviews. Rheumatology · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. T cell plasticity in renal autoimmune disease.Cell and tissue research · 2021
    Review
  12. Microbiota, renal disease and renal transplantation.World journal of transplantation · 2021
    Review
  13. Article
  14. Article
  15. Frontiers in immunology · 2021
    Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Role of MicroRNAs in Renal Parenchymal Diseases-A New Dimension.International journal of molecular sciences · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Christian F KrebsIII Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany;
Sonja Kapffer
Hans-Joachim Paust
Tilman Schmidt
Sabrina B Bennstein
Anett Peters
Gesa Stege
Silke R Brix
Catherine Meyer-Schwesinger
Roman-Ulrich Müller
Jan-Eric Turner
Oliver M Steinmetz
Gunter Wolf
Rolf A K Stahl
Ulf Panzer
University Medical Center Hamburg-Eppendorf · DEUniversität Hamburg · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEJena University Hospital · DEMedical Research Council · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD4(+) T cells play a pivotal role in the pathogenesis of autoimmune disease, including human and experimental crescentic GN. Micro-RNAs (miRs) have emerged as important regulators of immune cell development, but the impact of miRs on the regulation of the CD4(+) T cell immune response remains to be fully clarified. Here, we report that miR-155 expression is upregulated in the kidneys of patients with ANCA-associated crescentic GN and a murine model of crescentic GN (nephrotoxic nephritis). To elucidate the potential role of miR-155 in T cell-mediated inflammation, nephritis was induced in miR-155(-/-) and wild-type mice. The systemic and renal nephritogenic TH17 immune response decreased markedly in nephritic miR-155(-/-) mice. Consistent with this finding, miR-155-deficient mice developed less severe nephritis, with reduced histologic and functional injury. Adoptive transfer of miR-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag-1(-/-)) mice showed the T cell-intrinsic importance of miR-155 for the stability of pathogenic TH17 immunity. These findings indicate that miR-155 drives the TH17 immune response and tissue injury in experimental crescentic GN and show that miR-155 is a potential therapeutic target in TH17-mediated diseases.

Indexed as

AnimalsCells, CulturedDisease Models, AnimalGlomerulonephritisHumansImmunity, HumoralImmunophenotypingMaleMiceMice, CongenicMice, Inbred C57BLMice, Mutant StrainsMicroRNAsNeutrophilsSpleenTh17 CellsMicroRNAsMIRN155 microRNA, humanMirn155 microRNA, mouse

Identifiers

PMID23949802
PMCPMC3839549
OpenAlexW2041322441

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.