ArticleCellular oncology (Dordrecht, Netherlands)2023
TNFR2 antagonistic antibody induces the death of tumor infiltrating CD4
Article in Cellular oncology (Dordrecht, Netherlands), 2023. 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
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Mapping the TNFR2-targeting antibody patent landscape: Insights from macro trends to structural signatures.Human vaccines & immunotherapeutics · 2026Article
- TRIP13 promotes the expansion and immunosuppression of CD4Cell death & disease · 2026Article
- Review
- Therapeutic potential of TNFR2 agonists: a mechanistic perspective.Frontiers in immunology · 2023Review
- TNFR2 expression predicts the responses to immune checkpoint inhibitor treatments.Frontiers in immunology · 2023Article
- Ansofaxine hydrochloride inhibits tumor growth and enhances Anti-TNFR2 in murine colon cancer model.Frontiers in pharmacology · 2023Article
- Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundTNFR2 expression is a characteristic of highly potent immunosuppressive tumor infiltrating CD4
methodTY101, an anti-murine TNFR2 antibody, was used to examine the effect of TNFR2 blockade on Treg proliferation and viability in vitro. The role of TNFR2 on Treg viability was further validated by TNFR2 knockout mice and in the TY101 antagonistic antibody-treated mouse tumor model.
resultsIn this study, we found that an anti-mouse TNFR2 antibody TY101 could inhibit TNF-induced proliferative expansion of Tregs, indicative of an antagonistic property. To examine the effect of TY101 antagonistic antibody on Treg viability, we treated unfractionated lymph node (L.N.) cells with Dexamethasone (Dex) which was known to induce T cell death. The result showed that TY101 antagonistic antibody treatment further promoted Treg death in the presence of Dex. This led us to find that TNFR2 expression was crucial for the survival of Tregs. In the mouse EG7 lymphoma model, treatment with TY101 antagonistic antibody potently inhibited tumor growth, resulting in complete regression of the tumor in 60% of mice. The treatment with TY101 antagonistic antibody elicited potent antitumor immune responses in this model, accompanied by enhanced death of Tregs.
conclusionThis study, therefore, provides clear experimental evidence that TNFR2 antagonistic antibody, TY101, can promote the death of Tregs, and this effect may be attributable to the antitumor effect of TNFR2 antagonistic antibody.
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Registered trials
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