ArticleTheranostics2026
A nanoengineered MSC therapeutic for synergistic therapy of lupus nephritis via cfDNA clearance and targeted immunomodulation.
Article in Theranostics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rationale: Lupus nephritis (LN) remains a clinical challenge due to the dose-limiting toxicity of conventional immunosuppressants and the poor engraftment/efficacy of mesenchymal stromal cell (MSC) therapies. Methods: We report a novel nanoengineered MSC therapeutic for LN by engineering MSCs with a cell-free DNA (cfDNA)-targeting dendritic nanogel. To obtain the hybrid MSC-G3K@T system, we coupled tacrolimus-loaded, disulfide-crosslinked polylysine dendrimer nanogels (G3K@T) onto the MSC membrane. Our system exploits two synergistic targeting strategies: the innate homing capacity of MSCs, plus the specific affinity of the cationic G3K dendrimer for anionic cfDNA, which enriches in inflamed kidneys. Results: Our system acts through two coordinated actions: the nanogel responds to the oxidative renal microenvironment and releases tacrolimus in a spatiotemporally controlled manner, thereby suppressing T-cell activation. At the same time, it scavenges cfDNA, blocking TLR-mediated pro-inflammatory signaling. Working together with the inherent immunomodulatory functions of MSCs, this dual-action strategy yielded robust efficacy in MRL/lpr mice, including a significant reversal of T-cell dysregulation, restoration of glomerular integrity, and reduction of proteinuria and IgG deposition. Conclusions: We propose that MSC-G3K@T offers a promising route to augment cell-based therapies, creating a versatile platform that could be used to treat autoimmune and inflammatory diseases.
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.