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. Author manuscript; available in PMC: 2020 May 18.
Published in final edited form as: Bioconjug Chem. 2018 Oct 24;29(12):3937–3966. doi: 10.1021/acs.bioconjchem.8b00548

Figure 4. Passive immunotherapy strategies for brain cancer using immune checkpoint inhibitory antibodies.

Figure 4.

Interactions between T cells, antigen presenting cells (APCs), and tumor cells that inhibit appropriate activation of T cell cytotoxic immune responses may be modulated via passive immunotherapy. For example, anti-PD-1 antibodies can bind to the PD-1 receptor that is expressed by T cells and disrupt PD-1’s interaction with its ligand PD-L1, which is highly expressed on tumor cells and APCs in the tumor microenvironment. Alternatively, anti-PD-L1 antibodies can neutralize the PD-L1 ligand’s ability to bind to PD-1. Anti-CTLA-4 antibodies may be used to block the interaction between the CTLA-4 receptor on Treg cells and the B7 ligand on tumor cells and APCs; this would subsequently allow B7 interaction with the CD28 receptor on T cells, which provides a stimulatory signal for T cell activation. Adapted from: 53–55. Abbreviations: PD-1 – programmed cell death protein-1; PD-L1 – programmed cell death protein ligand-1; CTLA-4 – cytotoxic T-lymphocyte-associated protein 4; Treg – regulatory T cells; CD28 – classification determinant 28.