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. 2022 Mar 16;79(3):191. doi: 10.1007/s00018-022-04219-z

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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/.

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Fig. 3 — The effects of type I IFNs in the TME. Type I IFNs induce tumor cell apoptosis and inhibit tumor cell proliferation and metastasis. In addition, type I IFNs upregulate TAA and MHC I expression in tumor cells. Type I IFNs are essential for NK cell maturation and activation. Moreover, type I IFNs increase NK cell cytotoxicity. Type I IFNs promote DC differentiation, maturation, and migration into lymph nodes to activate CD8⁺ T cells. Moreover, type I IFNs increase DC intratumoral accumulation. Type I IFNs reduce Treg infiltration into tumor and Treg proliferation. Type I IFNs inhibit neutrophil infiltration, longevity, and chemokine production. In addition, type I IFNs decrease differentiation and maturation of MDSCs, and block their suppressive activity on CD8⁺ T cells