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. 2023 Nov 27;22:187. doi: 10.1186/s12943-023-01885-w

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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. 6 — Harnessing innate immunity to improve antitumor immune response. The involvement of innate immunity is crucial for initiating and sustaining adaptive immunity, and it plays a significant role in the overall cancer-immunity cycle. When a tumor is detected, innate immune cells are activated, leading to the enhancement of their effector functions and the destruction of tumor cells. Apart from directly killing tumor cells, innate immune cells participate in priming, expanding, and infiltrating tumor-specific T-cells. Manipulating innate immunity by therapeutic strategies could effectively stimulate antitumor immune response and overcome immune evasion. Abbreviations: DC, dendritic cell; TAM, tumor-associated macrophage; NK cell, natural killer cell; MDSC, myeloid-derived suppressor cell; TME, tumor microenvironment; TCR, T cell receptor; MHC, major histocompatibility complex