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Phenotypic screening reveals TNFR2 as a promising target for cancer immunotherapy.

Title: Phenotypic screening reveals TNFR2 as a promising target for cancer immunotherapy.
Authors: Williams, Geoffrey S; Mistry, Bina; Guillard, Sandrine; Ulrichsen, Jane Coates; Sandercock, Alan M; Wang, Jun; González-Muñoz, Andrea; Parmentier, Julie; Black, Chelsea; Soden, Jo; Freeth, Jim; Jovanović, Jelena; Leyland, Rebecca; Al-Lamki, Rafia S; Leishman, Andrew J; Rust, Steven J; Stewart, Ross; Jermutus, Lutz; Bradley, John R; Bedian, Vahe; Valge-Archer, Viia; Minter, Ralph; Wilkinson, Robert W
Publisher Information: Impact Journals; //www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=11943&path%5B%5D=37807
Publication Year: 2016
Collection: Apollo - University of Cambridge Repository
Subject Terms: TNFR2; cancer immunotherapy; drug discovery; phenotypic screening; regulatory T cell; Animals; Antineoplastic Agents; Cell Line; Tumor; Drug Screening Assays; Antitumor; Female; HEK293 Cells; Humans; Immunotherapy; Jurkat Cells; Mice; Inbred BALB C; NF-kappa B; Neoplasms; Experimental; Phenotype; Receptors; Tumor Necrosis Factor; Type II; Signal Transduction; T-Lymphocytes; Regulatory
Description: Antibodies that target cell-surface molecules on T cells can enhance anti-tumor immune responses, resulting in sustained immune-mediated control of cancer. We set out to find new cancer immunotherapy targets by phenotypic screening on human regulatory T (Treg) cells and report the discovery of novel activators of tumor necrosis factor receptor 2 (TNFR2) and a potential role for this target in immunotherapy. A diverse phage display library was screened to find antibody mimetics with preferential binding to Treg cells, the most Treg-selective of which were all, without exception, found to bind specifically to TNFR2. A subset of these TNFR2 binders were found to agonise the receptor, inducing iκ-B degradation and NF-κB pathway signalling in vitro. TNFR2 was found to be expressed by tumor-infiltrating Treg cells, and to a lesser extent Teff cells, from three lung cancer patients, and a similar pattern was also observed in mice implanted with CT26 syngeneic tumors. In such animals, TNFR2-specific agonists inhibited tumor growth, enhanced tumor infiltration by CD8+ T cells and increased CD8+ T cell IFN-γ synthesis. Together, these data indicate a novel mechanism for TNF-α-independent TNFR2 agonism in cancer immunotherapy, and demonstrate the utility of target-agnostic screening in highlighting important targets during drug discovery. ; GW, BM, SG, JC-U, AS, AG-M, CB, JJ, RL, AJL, SR, RS, LJ, VV-A, RM and RWW were funded by MedImmune; JP and VB were funded by AstraZeneca PLC; JW, RSA-L and JB were funded by NIHR Cambridge Biomedical Research Centre and Kidney Research UK; JS and JF were funded by Retrogenix Ltd.
Document Type: article in journal/newspaper
File Description: application/pdf
Language: English
Relation: https://www.repository.cam.ac.uk/handle/1810/278311
DOI: 10.17863/CAM.24987
Availability: https://www.repository.cam.ac.uk/handle/1810/278311; https://doi.org/10.17863/CAM.24987
Rights: Attribution 4.0 International ; http://creativecommons.org/licenses/by/4.0/
Accession Number: edsbas.BAB21BD
Database: BASE