Evidence map›Paper›PMID 41796358›Full record

ArticleJournal of nanobiotechnology2026

Microneedle-based delivery of cell membrane vesicles as IL-17RA decoys for Psoriasis treatment.

Bin Tu, Weifeng Fang, Lin Liu, Yao Sun, Mei Hu, Akmal Asrorov, Zhao Wang, Ergang Liu, Yongzhuo Huang, Zhongqiu Liu and 1 more

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Bin Tu *Hospital Preparation Transformation Branch, Zhongshan Hospital of Traditional Chinese Medicine, The Tenth Clinical Medical College of Guangzhou University of Chinese Medicine, National Engineering Research Center for Modernization of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Zhongshan, 528400, China.
Weifeng Fang *Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Lin Liu *Zhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Yao SunZhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Mei HuHospital Preparation Transformation Branch, Zhongshan Hospital of Traditional Chinese Medicine, The Tenth Clinical Medical College of Guangzhou University of Chinese Medicine, National Engineering Research Center for Modernization of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Zhongshan, 528400, China.
Akmal AsrorovZhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Zhao WangXiangya School of Pharmaceutical Sciences, Central South University, Changsha, 410013, China.
Ergang LiuZhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China.
Yongzhuo HuangZhongshan Institute for Drug Discovery, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Zhongshan, 528400, China. yzhuang@simm.ac.cn.
Zhongqiu LiuState Key Laboratory of Traditional Chinese Medicine Syndrome, International Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. liuzq@gzucm.edu.cn.
Weibo DaiHospital Preparation Transformation Branch, Zhongshan Hospital of Traditional Chinese Medicine, The Tenth Clinical Medical College of Guangzhou University of Chinese Medicine, National Engineering Research Center for Modernization of Traditional Chinese Medicine, Guangzhou University of Chinese Medicine, Zhongshan, 528400, China. daiweibo007@163.com.

Funding

CAS President's International Fellowship Initiative 2024VBB0004he Grand Challenges and Future Network of the International Partnership Program of the Chinese Academy of Sciences 083GJHZ2023021GC & 083GJHZ2023012FNHigh-level Innovative Research Institute from Department of Science and Technology of Guangdong Province 2021B0909050003Medical Scientific Research Foundation of Guangdong Province B2025211National Key Research and Development Program of China 2025YFE0107400National Natural Science Foundation of China 82341232Natural Science Foundation of Shanghai Municipal 24ZR1477500University-Hospital Joint Fund Project of Guangzhou University of Chinese Medicine GZYZS2024D05Zhongshan Municipal Bureau of Science and Technology LJ2021001 & CXTD2022011
6 · The paper itself

Abstract

The dysregulation of IL-17/IL-17 receptor A (IL-17RA) signaling axis is a central driver of multiple autoimmune diseases. In contrast to targeting individual IL-17 cytokines, blocking IL-17RA simultaneously inhibits the receptor engagement of multiple IL-17 ligands, thereby effectively suppressing downstream pathway activation. Brodalumab, the only approved IL-17RA-blocking antibody, suggests robust clinical efficacy. However, its inhibition of IL-17RA has been associated with an increase in systemic IL-17 C levels, which is related to suicidal ideation and behavior. Consequently, the development of novel strategies capable of broadly blocking IL-17 signaling remains critically important. This study developed a novel therapeutic strategy by engineering cell-membrane vesicles with IL-17RA (IL-17RA-CMVs) as high-avidity decoy receptors for effectively blocking the IL-17/IL-17 receptor A (IL-17RA) signaling axis. Stable 293T cell lines exhibiting high surface expression of mouse or human IL-17RA (m/hIL-17RA), mediated by a platelet-derived growth factor receptor (PDGFR) transmembrane domain, were successfully constructed and applied for the preparation of m/hIL-17RA-CMVs. The mIL-17RA-CMVs were efficiently loaded into hyaluronic acid-based microneedles (mIL-17RA-CMVs-MNs), and the resulting mIL-17RA-CMVs-MNs exhibited sufficient mechanical strength to penetrate the skin and rapidly dissolved within 5 min upon insertion. In an imiquimod (IMQ)-induced murine psoriasis model, the topical application of mIL-17RA-CMVs-MNs significantly alleviated disease severity, as evidenced by a remarkable reduction in Psoriasis Area and Severity Index (PASI) scores, suppression of epidermal hyperplasia, and normalization of spleen index. Mechanistic studies revealed that the treatment mIL-17RA-CMVs-MNs markedly downregulated the expression of key IL-17RA pathway-related inflammatory mediators (CXCL1, CXCL2, CCL20) and antimicrobial peptides (S100A7/A8/A9) in skin lesions. Furthermore, in vitro experiments indicated that hIL-17RA-CMVs effectively functioned as decoy receptors, neutralizing IL-17 A and consequently inhibiting the upregulation of pro-inflammatory cytokines and hyperproliferation in HaCaT keratinocytes. This study presents a pioneering approach that synergizes the broad-spectrum neutralization capability of engineered decoy receptor vesicles with the localized and minimally invasive delivery advantage of microneedles. These findings position IL-17RA-CMVs (or IL-17RA-CMVs-MNs) as a highly promising and translatable therapeutic modality for the treatment of psoriasis and potentially other IL-17-mediated inflammatory diseases.

Indexed as

Cell MembranePsoriasisReceptors, Interleukin-17AnimalsAntibodies, Monoclonal, HumanizedFemaleHEK293 CellsHumansImiquimodInterleukin-17MiceMicroneedle Drug DeliverySignal TransductionAntibodies, Monoclonal, HumanizedbrodalumabIL17RA protein, humanImiquimodInterleukin-17Receptors, Interleukin-17Cell-membrane vesiclesDecoy receptorIL-17RAMicroneedlesPsoriasis

Identifiers

PMID41796358
PMCPMC13081452

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Registered trials

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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.