Evidence map›Paper›PMID 26631756›Full record

ArticleClinical immunology (Orlando, Fla.)2016

MicroRNA-21 deficiency protects from lupus-like autoimmunity in the chronic graft-versus-host disease model of systemic lupus erythematosus.

Barry Garchow, Marianthi Kiriakidou

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Therapeutic Applications of Poly-miRNAs and miRNA Sponges.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Review
  4. Lupus Nephritis from Pathogenesis to New Therapies: An Update.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Non-Coding RNAs in CD4Frontiers in immunology · 2020
    Review
  11. MicroRNAs in Autoimmunity and Hematological Malignancies.International journal of molecular sciences · 2018
    Review
  12. Review
  13. Tregs in SLE: an Update.Current rheumatology reports · 2018
    Review
  14. Regulatory T cells in renal disease.Clinical & translational immunology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Barry GarchowDepartment of Medicine, Division of Rheumatology, Sidney Kimmel Medical College, Thomas Jefferson University, 211 S. 9th St. Suite 210, Philadelphia, PA 19107, USA.
Marianthi KiriakidouDepartment of Medicine, Division of Rheumatology, Sidney Kimmel Medical College, Thomas Jefferson University, 211 S. 9th St. Suite 210, Philadelphia, PA 19107, USA. Electronic address: marianthi.kiriakidou@jefferson.edu.
Thomas Jefferson University · US

Funding

Effects of miR-21 and miR-155 inhibition in SLER21AR063416 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI KIRIAKIDOU, MARIANTHI · 2013 to 2014
$368k
Characterization of microRNA-regulated signaling pathways in mouse SLER03AR060988 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI KIRIAKIDOU, MARIANTHI · 2011 to 2013
$272k
NIAMS NIH HHS R03 AR060988NIAMS NIH HHS R21 AR063416
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small, non-coding RNAs that regulate gene expression primarily at the post-transcriptional level. Emerging evidence supports a regulatory role for miRNAs in the immune response and autoimmunity. In this work, we investigated the implication of miR-21 in the experimentally inducible bm12→B6 cGVHD model of systemic lupus erythematosus (SLE). cGVHD host mice deficient in miR-21 show a 2-fold reduction in splenomegaly, significantly reduced autoantibody titers and down-regulated components of the CD40:CD40L and CD28:CD80/86 co-stimulation pathways. Furthermore, we demonstrate that miR-21-deficient hosts have reduced CD4(+) IL-17(+) cell populations and an expanded CD4(+) CD25(+) FoxP3(+) cell compartment. We propose that miR-21 has a pluripotent role, serving to link distinct lymphocyte signaling pathways and acting as a "rheostat" for signals that promote B and T cell activation in lupus. Collectively, our experiments demonstrate that miR-21 deficiency in cGVHD host mice is sufficient to protect from lupus-like autoimmunity.

Indexed as

Graft vs Host DiseaseAnimalsAutoimmunityDisease Models, AnimalFlow CytometryHumansLupus Erythematosus, SystemicMiceMicroRNAsMicroRNAsAutoantibodiesAutoimmunityB cellscGVHDCo-stimulatory pathwaysCytokinesIL-17LupusLupus nephritisMicroRNAMiR-21SLESplenomegalyT cellsTh17Tregs

Identifiers

PMID26631756
PMCPMC6527104
OpenAlexW2174420509

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.