ArticleJournal of advanced research2026
Basophilic exosomes promote SLE development via exacerbating B cell activation through the lncRNA ENST00000537616/miR-330-5p/KRAS axis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Hsa_circ_0065149 mediates the ceRNA network pathway: Research on the mechanism regulating myasthenia gravis.Journal of molecular neuroscience : MN · 2026Article
- Exosomal non-coding RNAs in autoimmune diseases: molecular mechanisms and potential applications.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionUncontrolled B-cell activation in systemic lupus erythematosus (SLE) induces autoantibody production and inflammation and causes tissue damage. Basophils have been shown to promote B cell activation in SLE; however, the molecular mechanisms involved remain nebulous.
objectiveTo elucidate the role of basophilic exosomes in B-cell activation and explore the associated molecular mechanisms in SLE.
methodsWe employed a multifaceted approach combining human cell studies and animal models and assessed the effects of human basophil-derived exosomes on B cell activation in SLE patients by evaluating activation markers following exosome uptake. Furthermore, we used a basophil-depleted lupus mouse model to examine the impact of basophilic exosomes on disease progression and conducted transcriptomic analysis of basophilic exosomes to identify key molecular regulators. Finally, we explored the therapeutic potential of targeting lncRNA ENST00000537616 by intervening in its expression in humanized SLE mouse models.
resultsHuman-activated basophil-derived exosomes significantly enhanced the activation of B cells from SLE patients in vitro. In the basophil-depleted lupus mouse model, activated basophilic exosomes induced excessive splenic immune cell proliferation and exacerbated renal dysfunction. Transcriptomic analysis revealed lncRNA ENST00000537616 as a key regulator released by activated basophilic exosomes, promoting B cell activation. LncRNA ENST00000537616 inhibition in a humanized SLE mouse model significantly attenuated immune hyperactivation and improved renal function, mirroring the effects of activated basophilic exosome inhibition. Mechanistically, activated basophilic exosomes facilitated B cell activation via the lncRNA ENST00000537616/miR-330-5p/KRAS axis.
conclusionsThis study provides novel insights into the pathogenesis of SLE by elucidating the role of basophilic exosomes and the lncRNA ENST00000537616/miR-330-5p/KRAS axis in B cell activation.
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.