Figures & data
Figure 1 Immune checkpoint inhibitors in cancer treatment.
Notes: Inability to activate CTLs in tumor microenvironment through the suppressive effect of Tregs or through immune checkpoints allows cancer cells to escape immune attack, survive, and grow. B7 ligands expressed on antigen-presenting cells bind to CD28 receptor on CTL leading to T cell amplification and immune response. Alternatively, binding of B7 ligands to CTLA-4 expressed on T cells suppresses their activity. CTLA-4 also enhances the activity of Tregs leading to immunosuppressive activity. PD-1 is expressed on activated T cells. PD-1 binds to its PD-L1 leading to the anergy of CTLs further promoting inhibitory signals. Pharmacological inhibition of immune checkpoints with monoclonal antibodies restores CTL antitumor activity and relieves immunosuppression.
Abbreviations: CTLA-4, cytotoxic T-lymphocyte antigen 4; CTLs, cytotoxic T lymphocytes; DC, dendritic cell; MHC, major histocompatibility complex; PD-1, programmed cell death-1; PD-L1, programmed cell death-1 ligand; TCR, T cell receptor; Tregs, regulatory T cells.
Abbreviations: CTLA-4, cytotoxic T-lymphocyte antigen 4; CTLs, cytotoxic T lymphocytes; DC, dendritic cell; MHC, major histocompatibility complex; PD-1, programmed cell death-1; PD-L1, programmed cell death-1 ligand; TCR, T cell receptor; Tregs, regulatory T cells.
Table 1 Ongoing clinical trials of CTLA-4 inhibitor immunotherapeutics in breast cancer
Table 2 Ongoing clinical trials of PD-1/PD-L1 immunotherapeutics in breast cancer
Table 3 Ongoing clinical trials of peptide- and DC-based vaccine immunotherapeutics in breast cancer