ArticleAllergy2025
Feedback regulation of VISTA and Treg by TNF-α controls T cell responses in drug allergy.
Article in Allergy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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
5 citing papers in PubMed.
- New Insights Into Immunomodulatory Strategies for Drug Hypersensitivity Reactions: An EAACI Task Force Report.Clinical and translational allergy · 2026Review
- Insights into the Biochemical and Immune Mechanisms in Drug-Induced Liver Injury Pathogenesis.Chemical research in toxicology · 2026Review
- Association of decreased CYP2C9 function,Frontiers in pharmacology · 2026Article
- TSC22 domain family member 3 links natural killer cells to CD8+ T cell-mediated drug hypersensitivity.Signal transduction and targeted therapy · 2025Article
- Feedback regulation of VISTA and Treg by TNF-α controls T cell responses in drug allergy.Allergy · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
backgroundSevere cutaneous adverse reactions (SCARs) mediated by cytotoxic T lymphocytes are a series of life-threatening conditions with a mortality of 4%-20%. The clinical application of tumor necrosis factor-alpha (TNF-α) antagonist improves the outcome of some SCARs patients; however, this is complicated by the elusive and varied immunopathogenesis.
methodsTo clarify the precise process and optimize the therapy regimen of SCARs, we performed single-cell sequencing, in vitro functional and clinical analysis of patients with SCARs.
resultsWe observed that TNF-α breaks drug-specific T-cell tolerance by inhibiting the expression of V-type immunoglobulin domain-containing suppressor of T-cell activation (VISTA). Furthermore, TNF-α generated a positive feedback loop in the early phase of drug-specific T-cell activation, whereby B cells acted reciprocally on the corresponding T cells to reinforce TNF-α cytokine expression. In contrast, this pathway of TNF-α-VISTA signaling did not operate in memory effector T cells. Drug-specific memory effector T-cell responses were inhibited by increasing Treg cell expression in a negative feedback loop, with TNF-α antagonists preventing the inhibitory effect. These observations align with the clinical analysis that early but not late intervention with TNF-α antagonists significantly improved outcomes in SCARs patients.
conclusionOur findings defining feedback regulation of VISTA and Treg cells by TNF-α in different stages of the drug-specific T-cell response and, indicate that a Treg agonists, instead of TNF-α antagonists, could be used for treatment of patients with progressive SCARs.
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