Evidence map›Paper›PMID 42479022›Full record

ArticleInvestigative ophthalmology & visual science2026

VISTA Deficiency Exacerbates Autoimmune Uveitis by Promoting Microglial Activation via the TLR4/MyD88/NF-κB Pathway.

Hui Feng, Baorui Chu, Xianyang Liu, Chao Wu, Fan Cao, Shuhao Zeng, Yakun Wang, Xinyuan Chen, Shangze Gao, Wenxian Yang and 3 more

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In one paragraph

Article in Investigative ophthalmology & visual science, 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
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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

13 authors.

Hui FengBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Baorui ChuDepartment of Ophthalmology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Xianyang LiuBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Chao WuBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Fan CaoBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Shuhao ZengBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Yakun WangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Xinyuan ChenBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Shangze GaoBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Wenxian YangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Hui YangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Hong WangBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Shengping HouBeijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: VISTA, an immune checkpoint enriched in microglia, regulates inflammatory signaling. Given microglial activation drives autoimmune uveitis, we investigated whether VISTA protects against experimental autoimmune uveitis (EAU) by modulating retinal microglia. Methods: VISTA expression was analyzed by flow cytometry in active VKH patients and healthy controls. Functional studies in LPS/IFN-γ-stimulated BV2 microglia used genetic knockdown/overexpression and modulating antibodies (13F3, MH5A). Activation status, cytokine secretion, migration, and TLR4/MyD88/NF-κB signaling were assessed. An EAU mouse model received intravitreal adeno-associated virus-mediated VISTA overexpression, with severity evaluated clinically and histopathologically. Results: VISTA was downregulated in circulating immune cells of VKH patients and in retinal microglia during EAU. In vitro, inflammatory stimuli reduced microglial VISTA. Its knockdown or blockade exacerbated microglial activation, pro-inflammatory mediator secretion (TNF-α, iNOS, COX2), and migration, while overexpression or agonism suppressed activation. Critically, intravitreal VISTA overexpression alleviated EAU severity. Mechanistically, VISTA deficiency potentiated activation by enhancing TLR4/MyD88/NF-κB signaling. Conclusions: VISTA is a crucial gatekeeper of ocular immune homeostasis. Its downregulation promotes uveitis via microglial TLR4/MyD88/NF-κB pathway activation, making VISTA signaling restoration a promising therapeutic strategy.

Indexed as

Autoimmune DiseasesMicrogliaMyeloid Differentiation Factor 88NF-kappa BToll-Like Receptor 4UveitisAnimalsDisease Models, AnimalFemaleFlow CytometryHumansMaleMiceMice, Inbred C57BLSignal TransductionMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID42479022
PMCPMC13399068

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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.