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. 2022 Oct 31;3(5):676–693. doi: 10.37349/etat.2022.00107

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Figure 3. — Scheme of CTLA-4 blockade. Tumor cells “hijack” immune checkpoints to disable host immunity. Illustrated are the schemes of an APC attempting to present tumor-associated antigens to T cells. However, with normal immunity, the CD28 co-activating receptors on T cells would be bound to B7 proteins on APCs except for the checkpoint braking effect, e.g., by CTLA-4. When CTLA-4 binds to B7, the host immunity effect is disabled. Upon administering an anti-CTLA-4 (an ICB), the effect would be reversed, i.e., no more braking effect as B7 is now bound to CD-28 again, clearly to the tumor cells’ great disappointment [16]. APC: antigen-presenting cell; CTLA-4: cytotoxic T-lymphocyte-associated-4; “↔”: binding to