ArticleJCI insight2020
MicroRNA-148a facilitates inflammatory dendritic cell differentiation and autoimmunity by targeting MAFB.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular Signature and miRNA Pattern of CD4 + T Lymphocytes in Plaque Psoriasis.Clinical reviews in allergy & immunology · 2026Review
- Cutaneous Dendritic Cells: Structure, Function and Immune Role.Biomedicines · 2026Review
- Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026Review
- Pre-Administration of Akkermansia Muciniphila Prevents the Development of Severe Acute Graft-Versus-Host Disease in Systemic Organs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Antisense oligonucleotides targeting IRF4 alleviate psoriasis.Acta pharmaceutica Sinica. B · 2025Article
- The effect of plasma exosomal microRNA- 148a- 3p on the CD4Archives of dermatological research · 2025Article
- Psoriasis Treatments: Emerging Roles and Future Prospects of MicroRNAs.Non-coding RNA · 2025Review
- Dairy: Friend or Foe? Bovine Milk-Derived Extracellular Vesicles and Autoimmune Diseases.International journal of molecular sciences · 2024Review
- Nonspecific Orbital Inflammation (NSOI): Unraveling the Molecular Pathogenesis, Diagnostic Modalities, and Therapeutic Interventions.International journal of molecular sciences · 2024Review
- RNA-Based Antipsoriatic Gene Therapy: An Updated Review Focusing on Evidence from Animal Models.Drug design, development and therapy · 2024Review
- A panel of blood-based circulatory miRNAs with diagnostic potential in patients with psoriasis.Frontiers in medicine · 2023Article
- MiR-148a deletion protects from bone loss in physiological and estrogen-deficient mice by targeting NRP1.Cell death discovery · 2022Article
- Milk Exosomal microRNAs: Postnatal Promoters of β Cell Proliferation but Potential Inducers of β Cell De-Differentiation in Adult Life.International journal of molecular sciences · 2022Review
- MicroRNA expression profiling of cerebrospinal fluid/serum exosomes in children with human herpesvirus 6-associated encephalitis/encephalopathy by high-throughput sequencing.Journal of neurovirology · 2022Article
- The role of a key transcription factor PU.1 in autoimmune diseases.Frontiers in immunology · 2022Review
- Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocyte-derived DCs (moDCs) have been implicated in the pathogenesis of autoimmunity, but the molecular pathways determining the differentiation potential of these cells remain unclear. Here, we report that microRNA-148a (miR-148a) serves as a critical regulator for moDC differentiation. First, miR-148a deficiency impaired the moDC development in vitro and in vivo. A mechanism study showed that MAFB, a transcription factor that hampers moDC differentiation, was a direct target of miR-148a. In addition, a promoter study identified that miR-148a could be transcriptionally induced by PU.1, which is crucial for moDC generation. miR-148a ablation eliminated the inhibition of PU.1 on MAFB. Furthermore, we found that miR-148a increased in monocytes from patients with psoriasis, and miR-148a deficiency or intradermal injection of antagomir-148a immensely alleviated the development of psoriasis-like symptoms in a psoriasis-like mouse model. Therefore, these results identify a pivotal role for the PU.1-miR-148a-MAFB circuit in moDC differentiation and suggest a potential therapeutic avenue for autoimmunity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.