Evidence map›Paper›PMID 29183643›Full record

ArticleJournal of autoimmunity2018

Selective targeting of pro-inflammatory Th1 cells by microRNA-148a-specific antagomirs in vivo.

Patrick Maschmeyer, Georg Petkau, Francesco Siracusa, Jakob Zimmermann, Franziska Zügel, Anja Andrea Kühl, Katrin Lehmann, Sarah Schimmelpfennig, Melanie Weber, Claudia Haftmann and 13 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of autoimmunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. The effect of plasma exosomal microRNA- 148a- 3p on the CD4Archives of dermatological research · 2025
    Article
  4. Overview of the Different Classes of Small RNAs During B-Cell Development.Methods in molecular biology (Clifton, N.J.) · 2025
    Review
  5. Review
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  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Murine T-Cell Transfer Colitis as a Model for Inflammatory Bowel Disease.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  16. Review
  17. Review
  18. Article
  19. Non-Coding RNAs in CD4Frontiers in immunology · 2020
    Review
  20. [New developments in topical pharmaceuticals].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2019
    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

23 authors at 5 institutions in 2 countries.

Patrick MaschmeyerDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Georg PetkauDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Francesco SiracusaDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Jakob ZimmermannDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Franziska ZügelDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Anja Andrea KühlCharité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin und Berlin Institute of Health, Campus Benjamin Franklin, Berlin, Germany.
Katrin LehmannDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Sarah SchimmelpfennigDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Melanie WeberDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Claudia HaftmannDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
René RiedelDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Markus BarduaDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Gitta Anne HeinzDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Cam Loan TranDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Bimba Franziska HoyerDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany; Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin und Berlin Institute of Health, Campus Benjamin Franklin, Berlin, Germany.
Falk HiepeDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany; Charité Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin und Berlin Institute of Health, Campus Benjamin Franklin, Berlin, Germany.
Sebastian HerzogDivision of Developmental Immunology, BIOCENTER, Medical University Innsbruck, Innsbruck, Austria.
Jürgen WittmannDivision of Molecular Immunology, Department of Internal Medicine III, Nikolaus-Fiebiger-Center, University of Erlangen-Nürnberg, Erlangen, Germany.
Nikolaus RajewskyBerlin Institute for Medical Systems Biology, Berlin, Germany.
Fritz Georg MelchersDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Hyun-Dong ChangDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Andreas RadbruchDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany.
Mir-Farzin MashreghiDeutsches Rheuma-Forschungszentrum Berlin (DRFZ), Germany. Electronic address: mashreghi@drfz.de.
German Rheumatism Research Centre · DEHumboldt-Universität zu Berlin · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEInnsbruck Medical University · ATMSB Medical School Berlin · DE

Funding

European Research Council 268987
6 · The paper itself

Abstract

In T lymphocytes, expression of miR-148a is induced by T-bet and Twist1, and is specific for pro-inflammatory Th1 cells. In these cells, miR-148a inhibits the expression of the pro-apoptotic protein Bim and promotes their survival. Here we use sequence-specific cholesterol-modified oligonucleotides against miR-148a (antagomir-148a) for the selective elimination of pro-inflammatory Th1 cells in vivo. In the murine model of transfer colitis, antagomir-148a treatment reduced the number of pro-inflammatory Th1 cells in the colon of colitic mice by 50% and inhibited miR-148a expression by 71% in the remaining Th1 cells. Expression of Bim protein in colonic Th1 cells was increased. Antagomir-148a-mediated reduction of Th1 cells resulted in a significant amelioration of colitis. The effect of antagomir-148a was selective for chronic inflammation. Antigen-specific memory Th cells that were generated by an acute immune reaction to nitrophenylacetyl-coupled chicken gamma globulin (NP-CGG) were not affected by treatment with antagomir-148a, both during the effector and the memory phase. In addition, antibody titers to NP-CGG were not altered. Thus, antagomir-148a might qualify as an effective drug to selectively deplete pro-inflammatory Th1 cells of chronic inflammation without affecting the protective immunological memory.

Indexed as

AnimalsAntagomirsCell DifferentiationCells, CulturedColitisColonDisease Models, AnimalHumansInflammationMiceMice, Inbred C57BLMicroRNAsNuclear ProteinsT-bet Transcription FactorT-Box Domain ProteinsTh1 Cellsantagomir-148aAntagomirsMicroRNAsMirn148 microRNA, mouseNuclear ProteinsT-bet Transcription FactorT-Box Domain ProteinsTWIST1 protein, humanTwist-Related Protein 1AntagomirsChronic inflammationInflammatory bowel diseasemiRNA-148aOligonucleotide therapyPre-clinical studyPro-inflammatory Th1 cells

Identifiers

PMID29183643
PMCPMC5916452
OpenAlexW2771066917

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.