Evidence map›Paper›PMID 40437612›Full record

ArticleCell communication and signaling : CCS2025

Identification of genetically engineered strategies to manipulate nano-platforms presenting immunotherapeutic ligands for alleviating primary ovarian insufficiency progression.

Guannan Zhou, Yuanyuan Gu, Menglei Zhang, Jingxin Ding, Guanming Lu, Keqin Hua, Fang Shen

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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

7 authors.

Guannan Zhou *Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai, 200011, People's Republic of China. zgnsmmu@163.com.
Yuanyuan Gu *Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai, 200011, People's Republic of China.
Menglei Zhang *Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai, 200011, People's Republic of China.
Jingxin Ding *Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai, 200011, People's Republic of China.
Guanming Lu *Department of Breast and Thyroid Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China.
Keqin Hua *Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai, 200011, People's Republic of China.
Fang Shen *Department of Gynecology, The Obstetrics and Gynecology Hospital of Fudan University, 419 Fang-Xie Road, Shanghai, 200011, People's Republic of China.

Funding

General program of Guangxi Natural Science Foundation No.2019JJA140071National Natural Science Foundation of China No.32060208, No.82260532National Natural Science Foundation of China No.81771524, No.81471416
6 · The paper itself

Abstract

Primary ovarian insufficiency (POI) is a pathological condition characterized by the early loss of functional ovarian follicles, leading to infertility and systemic consequences affecting reproductive, skeletal, cardiovascular, and neurocognitive helath. Aberrant immune activation, particularly an augmented T cell response in the ovary, plays a critical role in POI pathogenesis. In this context, therapeutic modulation of immune responses through immune checkpoint ligands has garnered interest. In the present study, we identified Lamp2b as an optimal scaffold for engineering extracellular vesicles (EVs). By genetically modifying HEK-293 T-derived EVs to present PD-L1 and Gal-9, enabling them to suppress ovarian autoreactive T lymphocytes and protect ovarian cells from immune-mediated destruction. Functionally, the bioengineered nanoplatform demonstrated potent immunosuppressive effects by promoting apoptosis of effector T cells, reducing intraovarian CD8⁺ T cell infiltration and reinstating serum anti-Müllerian hormone (AMH) levels in POI models. These combined actions effectively halted disease progression, ultimately preventing POI progression and preserving ovarian function.

Indexed as

Disease ProgressionGenetic EngineeringImmunotherapyPrimary Ovarian InsufficiencyAnimalsB7-H1 AntigenExtracellular VesiclesFemaleHEK293 CellsHumansLigandsMiceB7-H1 AntigenLigands

Identifiers

PMID40437612
PMCPMC12121283

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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.