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Updated: Aug 6, 2026
07:40
Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
VISTA Deficiency Exacerbates Autoimmune Uveitis by Promoting Microglial Activation via the TLR4/MyD88/NF-κB Pathway
Hui Feng1, Baorui Chu2, Xianyang Liu1
1Beijing Institute of Ophthalmology, Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Investigative Ophthalmology & Visual Science
|July 21, 2026
Summary
VISTA, an immune checkpoint protein, protects the eye from autoimmune uveitis by regulating microglia. Restoring VISTA function offers a potential therapy for this inflammatory eye disease.
Area of Science:
- Immunology
- Neuroscience
- Ophthalmology
Background:
- Microglial activation is a key driver of autoimmune uveitis.
- VISTA is an immune checkpoint protein found in microglia that regulates inflammatory signaling.
Purpose of the Study:
- To investigate if VISTA protects against experimental autoimmune uveitis (EAU) by modulating retinal microglia.
- To explore the role of VISTA in ocular immune homeostasis.
Main Methods:
- Analyzed VISTA expression in VKH patients and during EAU in mice.
- Conducted in vitro studies using BV2 microglia with VISTA knockdown/overexpression and antibody modulation.
- Assessed microglial activation, cytokine secretion, migration, and TLR4/MyD88/NF-κB signaling.
- Evaluated EAU severity in mice with VISTA overexpression.
Main Results:
- VISTA was downregulated in VKH patients and during EAU.
- In vitro, VISTA reduction worsened microglial activation and inflammation; VISTA increase suppressed it.
- VISTA deficiency enhanced TLR4/MyD88/NF-κB signaling in microglia.
- Overexpressing VISTA in the eye alleviated EAU severity.
Conclusions:
- VISTA is essential for maintaining ocular immune homeostasis.
- Downregulation of VISTA promotes uveitis through microglial TLR4/MyD88/NF-κB pathway activation.
- Restoring VISTA signaling presents a promising therapeutic strategy for uveitis.
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