ArticleJournal of leukocyte biology2024
TIGIT stimulation suppresses autoimmune uveitis by inhibiting Th17 cell infiltration.
Article in Journal of leukocyte biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Research Progress on the Regulatory Role of Treg Cells in Inflammatory Eye Diseases.Current issues in molecular biology · 2026Review
- Reduced TIGIT Expression on T Cells Links Hyperglycemia to Immune Dysregulation in Type 1 Diabetes.Cells · 2026Article
- Harnessing tumor immune checkpoints for autoimmune disease therapeutics.Frontiers in immunology · 2026Review
- Regulatory T cell dysfunction and exhaustion in uveitis: immunometabolic mechanisms, microenvironmental drivers, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- TIGIT/SHIP-1/RelB regulating Th1 inflammation in smoking induced COPD.Respiratory research · 2025Article
- Comparative models of uveitis.Eye (London, England) · 2025Review
- TIGIT deficiency promotes autoreactive CD4Nature communications · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
T cell immunoglobulin and ITIM domain (TIGIT) is an immune checkpoint molecule that suppresses T cell activation and promotes an immunosuppressive environment to suppress autoimmune diseases. However, the impact of a TIGIT agonist as a treatment for ocular autoimmune disease has not been investigated. We examined TIGIT expression on T helper 17 (Th17) and regulatory T cells (Tregs), the role of TIGIT on experimental autoimmune uveitis and Th17 cells, and the impact of Treg generation following TIGIT stimulation. TIGIT stimulation at the onset of clinical symptoms reduced the severity of uveitis and suppressed infiltration of Th17 cells into the eye. Further, Tregs from mice treated with the TIGIT agonist were capable of suppressing experimental autoimmune uveitis in recipient mice. This report demonstrates that stimulation of TIGIT at onset of disease suppresses symptoms and allows for induction of regulatory immunity that provides resistance to uveitis.
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Registered trials
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