Fig. 5
From: Advancements in clinical aspects of targeted therapy and immunotherapy in breast cancer
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