ArticleJournal of nanobiotechnology2026
MiR-1290 in natural killer cell derived extracellular vesicles: a pathogenic mediator of lupus nephritis and therapeutic target for th17 regulation.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
Abstract
Lupus nephritis (LN), a severe organ manifestation of systemic lupus erythematosus (SLE), is primarily driven by an imbalance between pathogenic Th17 cells and regulatory T (Treg) cells. We found that NK cell-derived extracellular vesicles (NK-EVs) from LN patients, but not healthy controls, exhibited a distinct miRNA cargo that potently drives Th17 polarization. Small RNA sequencing identified miR-1290 as the most significantly upregulated miRNA in NK-EVs derived from LN patients. This finding was validated in an independent clinical cohort, where miR-1290 levels correlated with key disease activity indices. Functional analysis revealed that miR-1290 promoted Th17 differentiation and suppressed Treg generation by downregulating NR4A2. In the MRL/lpr lupus mice, systemic delivery of NK-EVs engineered to carry a miR-1290 antagomir restored the Th17/Treg balance, alleviated renal inflammation and fibrosis. Collectively, we found miR-1290 in NK-EVs disrupted T cell homeostasis by targeting NR4A2, driving Th17/Treg imbalance. Delivering miR-1290 antagomirs via engineered NK-EVs restored this balance and alleviated renal damage in LN mice.
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.