ArticleJournal of nanobiotechnology2026
A combination therapy strategy: precision co-targeting of CCR7 and JAK1 with a smart hydrogel for inflammatory skin diseases.
Article in Journal of nanobiotechnology, 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
9 authors.
Funding
Abstract
Inflammatory skin diseases (ISDs) pose a major global burden, yet current therapies are limited by efficacy, accessibility, and cost, necessitating novel effective treatments. Thus, our study proposes a novel synergistic therapeutic strategy for psoriasis (PSO) and atopic dermatitis (AD) by concurrently targeting two critical pathological axes: immune cell chemotaxis via CCR7 inhibition and local inflammatory signaling via JAK1 suppression. A pH-responsive hydrogel (C-P@U/C-siCCR7) was designed for co-delivery of CCR7-targeting siRNA and the JAK1 inhibitor upadacitinib (UPA). Multi-omics analysis confirmed specific CCR7 overexpression in patient and model tissues. In vitro, the system inhibited keratinocyte proliferation, induced apoptosis, and downregulated key proteins in the JAK-STAT and PI3K/AKT/mTOR pathways along with pro-inflammatory cytokines. In IMQ-induced PSO and DNCB-induced AD mouse models, topical hydrogel application ameliorated skin lesions, restored the epidermal barrier, reduced hyperplasia and infiltration, and alleviated systemic immune activation-including suppression of splenomegaly and serum cytokines (IL17A, TNFα, IL4, IL13)-with favorable biosafety. The therapeutic effects were mechanistically linked to synergistic downregulation of CCR7, JAK1, STAT3, and mTOR in lesions, and reduced populations of aberrantly activated T cells, neutrophils, and dendritic cells in the spleen. This work provides a novel delivery platform and experimental evidence for developing effective, precise topical combination therapies against ISDs.
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.