Evidence map›Paper›PMID 41077603›Full record

ArticleScience China. Life sciences2026

Unveiling the choroidal immune landscape revealed interferon-gamma and TNF-alpha as novel therapeutic targets in dry AMD.

Lin Ye, Tujing Zhao, Huaping Tian, Runze Li, Zheng Li, Hongjing Li, Ruilin Liao, Junlan Chuan, Haojue Xu, Liang Zou and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Science China. Life sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Lin YeGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Tujing ZhaoGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Huaping TianGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Runze LiGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Zheng LiGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Hongjing LiGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Ruilin LiaoGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Junlan ChuanGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Haojue XuSichuan-Chongqing Joint Key Laboratory for Pathology and Laboratory Medicine, Jinfeng Laboratory, Chongqing, 401329, China.
Liang ZouSchool of Food and Biological Engineering, Chengdu University, Chengdu, 610106, China.
Chao QuDepartment of Ophthalmology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610075, China.
Yi ShiGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China.
Zhenglin YangGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China. yangzhenglin@cashq.ac.cn.
Lulin HuangGenetic Diseases Key Laboratory of Sichuan Province, Department of Laboratory Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 610054, China. huangluling@yeah.net.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age-related macular degeneration (AMD), particularly its atrophic (dry) form, is a leading cause of irreversible blindness in the elderly. Limited treatment efficacy stems from its complex pathogenesis, highlighting an urgent need for novel therapeutic targets. This study investigates the contribution of the choroidal immune microenvironment, focusing on intercellular communication involving resident fibroblasts-a cell type whose role in AMD remains poorly defined. By analyzing single-cell RNA sequencing data from human choroid, we interrogated crosstalk between fibroblasts, macrophages, and NK/T cells, identifying interferon-gamma (IFNγ) and tumor necrosis factor-alpha (TNFα) signaling pathways as central mediators. We demonstrate that activated choroidal fibroblasts release key inflammatory mediators, including IL6, CCL2, CSF1, CXCL9, and CXCL10, which functionally recruit macrophages and CD8

Indexed as

ChoroidInterferon-gammaMacular DegenerationTumor Necrosis Factor-alphaAnimalsDisease Models, AnimalFibroblastsHumansKiller Cells, NaturalMacrophagesMiceMice, Inbred C57BLSignal TransductionInterferon-gammaTumor Necrosis Factor-alphafibroblastsIFNγTAPI-1TNFαTofacitinib

Identifiers

PMID41077603

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.