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08-10-2018 | Image

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Figure 1: Mechanism of action for CTLA4, and PD1 or PDL1 immune checkpoint blockade therapy. a | The normal interaction of cytotoxic T-lymphocyte antigen 4 (CTLA4) with B7 co-stimulatory ligand is shown. The first activation signal is initiated when a T cell receptor (TCR) binds to the major histocompatibility complex (MHC) presenting an antigen on an antigen-presenting cell (APC) (1). A second activation signal is initiated when the CD28 receptor binds to B7 co-stimulatory ligand on the APC (2). CTLA4 receptors that are present on T cells function as a checkpoint and inhibit T cell activation by outcompeting CD28 receptors to bind to B7 ligand, which negates the effect of the second activation signal (3). b | Ipilimumab, a CTLA4 antibody, indirectly increases T cell activity by binding to the CTLA4 receptor. The second activation signal via B7 and CD28 connection is then reactivated. c | Tumour cells evade T cell detection by mimicking an APC with programmed cell death 1 ligand 1 (PDL1)-inhibiting ligand. This deactivates the T cell. d | By blocking either programmed cell death protein 1 (PD1) or PDL1 protein, nivolumab allows the T cell to detect tumour cells.

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