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. 2022 Mar 14;10:11. doi: 10.1186/s40364-022-00360-w

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© The Author(s) 2022

Open AccessThis 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. 2 — The regulatory and antitumor functions of DNTs. The antitumor functions of DNTs depend on expression of FasL, NKG2D, DNAM-1, TRAIL and NKp30. Moreover, secretion of IFN-γ, TNF-α, granzyme B and perforin take an important place. In addition, DNTs can mediate many types of immunocyte and exert immunoregulatory functions. DNTs downregulate expression of CD80/CD86 in dendritic cell and impact their interaction with other cells. DNTs can express MHC-peptide complex which expressed in dendritic cell by trogocytosis way, then interact with T cell and kill them through Fas/Fas L manner. Granzyme B and perforin secretion by DNTs induce death of T cell and B cell. Alternatively, DNTs kill M1 macrophage by down-regulating TNF-α and IFN-γ secretion of M1. FasL, Fas ligand; TNF-α, tumor necrosis factor α; NKG2D, natural killer group 2-member D; TRAIL: tumour necrosis factor-related apoptosis-inducing ligand