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. 2021 Jul 21;40(34):5253–5261. doi: 10.1038/s41388-021-01946-8

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© The Author(s) 2021

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Tumor cells may process and present tumor-specific or -associated antigens on MHC class I molecules through the MHC-I antigen processing pathway. CD8 T cells recognize tumor antigens presented by tumor cells and may secrete granzyme B (GrB) and perforin to mediate cytotoxicity toward tumor cells. In addition, dendritic cells (DCs), particularly the conventional DC1 (cDC1) subset, play several roles in helping CD4 and CD8 T cells to target tumors. 1 DCs may process and present or cross-present, shown in (a) tumor-derived MHC-I– and MHC-II–restricted tumor antigens to CD8 and CD4 T cells, respectively. T cells that can recognize tumor-specific neoantigens bind to the neoantigen peptide:MHC complex, and become activated, in a process termed T cell priming. 2 Activated CD4 T cells can “license” cDC1 cells through CD40:CD40L signals. 3 Subsequently, cDC1 cells can further enhance CD8 T cell activation. In addition to indirectly helping to boost CD8 responses through cDC1-mediated licensing, CD4 T cells can also provide direct help to augment CD8 T cell responses.