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. 2023 Aug 18;16:97. doi: 10.1186/s13045-023-01492-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 7 — Anti-tumor mode of CAR-γδT and CAR-NKT cell therapies. Both CAR-γδT and CAR-NKT cells can kill tumor cells through CAR-, ADCC-, Fas/FasL-, TRAIL-, and TNFR-mediated ways and can mobilize other immune cells by secreting cytokines. CAR-γδT cells can also be activated with select receptors, whereas the activating receptor of CAR-NKT cells is limited to CD1d. Furthermore, CAR-γδT cells can present antigens to T cells, and CAR-NKT cells can promote DC maturation and be activated by DCs. TAA, tumor-associated antigen; ADCC, FasL, Fas ligand; TRAILR, TRAIL receptor; TNFR, TNF receptor; TCR, T cell receptor; iTCR, invariant T cell receptor; CD40L, CD40 ligand; and DC, dendritic cell