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. 2023 Jul 6;22:105. doi: 10.1186/s12943-023-01805-y

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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. 5 — Immune escape mechanism of breast cancer cells and therapeutic role of immune checkpoint blockers in breast cancer treatment. When cytotoxic T-cells in the tumor microenvironment cannot be activated by immunological checkpoints or by the suppressive effect of Tregs, cancer cells are able to withstand the immune assault, survive, and proliferate. CTLA-4 is able to endorse Treg activity leading to an immunosuppressive effect. CTLA-4 binds to B7 (CD80 and CD86) expressed on APCs, such as DCs and inhibits T-cell-mediated immune response. In addition, the binding of CD28 with B7 on APCs suppresses T-cell activity. PD-1/PD-L1 system plays an important role later on and serves to abstract T-cell activity. When PD-1 binds to PD-L1, cytotoxic T-cells become anergic, which further encourages inhibitory signals. APC, Antigen presenting cell; CTLA-4, Cytotoxic T-lymphocytic antigen-4; DC, Dendritic cell; MHC, Major histocompatibility complex; PD-1, Programmed cell death-1; PD-L1. Programmed cell death-1 ligand; TCR: T-cell receptor; Treg, Regulatory T-cell