VISTA expression by microglia decreases during inflammation and is differentially regulated in CNS diseases
Open accessAbstract
V‐type immunoglobulin domain‐containing suppressor of T‐cell activation (VISTA) is a negative checkpoint regulator (NCR) involved in inhibition of T cell‐mediated immunity. Expression changes of other NCRs (PD‐1, PD‐L1/L2, CTLA‐4) during inflammation of the central nervous system (CNS) were previously demonstrated, but VISTA expression in the CNS has not yet been explored. Here, we report that in the human and mouse CNS, VISTA is most abundantly expressed by microglia, and to lower levels by endothelial cells. Upon TLR stimulation, VISTA expression was reduced in primary neonatal mouse and adult rhesus macaque microglia in vitro. In mice, microglial VISTA expression was reduced after lipopolysaccharide (LPS) injection, during experimental autoimmune encephalomyelitis (EAE), and in the accelerated aging Ercc1 Δ/− mouse model. After LPS injection, decreased VISTA expression in mouse microglia was accompanied by decreased acetylation of lysine residue 27 in histone 3 in both its promoter and enhancer region. ATAC‐sequencing indicated a potential regulation of VISTA expression by Pu.1 and Mafb, two transcription factors crucial for microglia function. Finally, our data suggested that VISTA expression was decreased in microglia in multiple sclerosis lesion tissue, whereas it was increased in Alzheimer's disease patients. This study is the first to demonstrate that in the CNS, VISTA is expressed by microglia, and that VISTA is differentially expressed in CNS pathologies.
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Vsir expression has been shown to be increased in several neurological diseases, such as Alzheimer's disease.
“Its expression has been shown to be increased in several neurological diseases, such as AD”
From Cross-Species Single-Cell Analysis Reveals Divergence of the Primate Microglia Program (2019) · cites this paper as Borggrewe et al., 2018
The Results and Discussion report elevated VISTA protein expression in microglia near plaques in one Alzheimer’s disease patient. They also report elevated expression in normal-appearing white matter from an MS patient, but reduced expression in chronic MS lesions. The evidence therefore supports the AD example, not a general increase across several neurological diseases; it measures VISTA protein rather than directly establishing increased Vsir gene expression. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPU.1 influences immune responses by regulating the expression of Aif1, Cx3cr1, Trem2, and Tyrobp.
“In addition, PU.1 influences immune responses by regulating the expression of allograft inflammatory factor 1 (Aif1, also known as ionized calcium‐binding adapter molecule 1, Iba1), C‐X3‐C motif chemokine receptor 1 (Cx3cr1), triggering receptor expressed on myeloid cells 2 (Trem2), and TYRO protein tyrosine kinase binding protein (Tyrobp) [32, 36].”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [36]
The Results section (page unavailable) identifies PU.1 binding motifs near the VISTA gene and says PU.1 is crucial for microglial function; the Discussion also calls it pivotal for microglial homeostasis. The paper does not say that PU.1 regulates Aif1, Cx3cr1, Trem2, or Tyrobp, so it does not support the claimed mechanism for influencing immune responses. (LLM, conf=0.78)
Experimental — accuracy not yet measuredVISTA functions as an inhibitory immune checkpoint, attenuating T-cell activation and contributing to immune homeostasis.
“VISTA functions as an inhibitory immune checkpoint, attenuating T‐cell activation and contributing to immune homeostasis. 49 , 50”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [49]
VISTA regulation may be disease- and context-dependent.
“suggesting that its regulation may be disease‐ and context‐dependent.”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [49]
VISTA has been reported to be upregulated in microglia surrounding Aβ plaques in AD but downregulated in chronically inflamed lesions in multiple sclerosis.
“VISTA has been reported to be upregulated in microglia surrounding Aβ plaques in AD but downregulated in chronically inflamed lesions in multiple sclerosis, 49”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [49]
MAFB has been implicated in regulation of the receptor VISTA in microglia.
“and in regulation of the receptor VISTA in microglia, which is upregulated in AD.82”
From Single nucleus multiomics identifies ZEB1 and MAFB as candidate regulators of Alzheimer’s disease-specific cis-regulatory elements (2023) · cites this paper as [82]
VISTA is upregulated in AD.
“and in regulation of the receptor VISTA in microglia, which is upregulated in AD.82”
From Single nucleus multiomics identifies ZEB1 and MAFB as candidate regulators of Alzheimer’s disease-specific cis-regulatory elements (2023) · cites this paper as [82]
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VISTA Expression on Cancer-Associated Endothelium Selectively Prevents T-cell Extravasation
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VISTA Emerges as a Promising Target against Immune Evasion Mechanisms in Medulloblastoma
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Characterisation of Immune Cell Subsets of Tumour Infiltrating Lymphocytes in Brain MetastasesPreprint
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Additional file 1 of IGSF11 and VISTA: a pair of promising immune checkpoints in tumor immunotherapy
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BindingDB (2024) · UC San Diego · doi:10.7270/q22j6h24
- Authors
- Borggrewe, M., Grit, C., Den Dunnen, W. F. A., Burm, S. M., Bajramovic, J. J., Noelle, R. J., Eggen, B. J. L., & Laman, J. D.
- Affiliations
- University Medical Center Groningen (NL)
- Department of Pathology, University of Groningen University Medical Center Groningen Groningen The Netherlands
- Biomedical Primate Research Centre (NL)
- Dartmouth College (US)
- Corresponding author
- Laman, Jon D.
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2018-10-11
- Volume
- 66
- Issue
- 12
- Pages
- 2645-2658
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC6585704
- OpenAlex
- W2896754653
- Cited by
- 91
- References
- 50
- Citations by year
- 2026: 12 · 2025: 7 · 2024: 15 · 2023: 18 · 2022: 16 · 2021: 14 · 2020: 6 · 2019: 3
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Glia (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion, cc-by)
- Funders
- Stichting MS Research (13‐833MS)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Keywords
- VISTA, microglia, T cell activation, neuroinflammation, lipopolysaccharide, experimental autoimmune encephalomyelitis, accelerated aging, histone H3K27 acetylation, PU.1, MAFB, multiple sclerosis, Alzheimer's disease, endothelial cells, transcriptional regulation
- MeSH terms
- Animals, Animals, Newborn, Brain, Calcium-Binding Proteins, Cells, Cultured, Central Nervous System Diseases, Disease Models, Animal, DNA-Binding Proteins, Endonucleases, Female, Freund's Adjuvant, Humans, Inflammation, Lipopolysaccharides, Macaca mulatta, Male, Membrane Proteins, Mice, Inbred C57BL, Mice, Transgenic, Microfilament Proteins, Nerve Tissue Proteins, Peptide Fragments, Gene Expression, Microglia, Mice, Myelin-Oligodendrocyte Glycoprotein
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