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. 2023 Aug 10;3(1):ltad013. doi: 10.1093/immadv/ltad013

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© The Author(s) 2023. Published by Oxford University Press on behalf of the British Society for Immunology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Combination therapies for BiTEs. A depiction of how BiTE combination strategies discussed. Single cell used to represent population of T cells and tumour cells for clarity. BiTE-induced tumour cell killing may be inhibited by immunosuppressive immune checkpoints, indicating that checkpoint inhibitors may synergise with BiTEs. Furthermore, pairing the traditional CD3xTAA BiTE with a CD28xTAA BiTE replicates costimulation (signal 2), leading to better T-cell activation directed towards tumour cells. Oncolytic viruses (OVs) has two distinct mechanisms. Firstly, viral oncolysis promotes inflammation (via the cancer-immunity cycle; Figure 1). Secondly, OVs can also be armed with BiTEs (OV-BiTEs), leading to selective delivery of a BiTE payload to tumour cells. OV-BiTEs may be targeted to tumour cells either by intratumoral injection (as depicted), or selective tropisms that limit replication exclusively to tumour cells. Produced using biorender.com.