Abstract
Re-engineering anti-CTLA-4 antibodies for enhancing cancer immunotherapy efficacy and safety.
Highlights
Cancers are able to progress by presenting receptors mimicking that of normal cells, i.e., tumor cells evade T cell detection by mimicking antigen-presenting cells (APCs) with programmed cell death 1 ligand (PD-L1)—inhibiting ligand, thence escaping immune detection [2]
Immunotherapeutic drugs are molecules administered to the patients to increase the sensitivity of these immune checkpoints, and immunotherapy has thereby revolutionized cancer treatment by reinforcing the host immune cells to target the cancer cells rather than directly targeting the cancer
From a more generalized perspective, irAEs occur in nearly 70% and 50% of those treated with anti-CTLA-4 and anti-PD-1/PD-L1 antibodies, respectively, due to the manipulation of the immune system to be more sensitive to these mimicked-receptors that bear high resemblance to innate ones, simultaneously unbalancing the regulatory mechanisms of self-tolerance [7,8]
Summary
From a more generalized perspective, irAEs occur in nearly 70% and 50% of those treated with anti-CTLA-4 and anti-PD-1/PD-L1 antibodies, respectively, due to the manipulation of the immune system to be more sensitive to these mimicked-receptors that bear high resemblance to innate ones, simultaneously unbalancing the regulatory mechanisms of self-tolerance [7,8].
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