New research suggests that dendritic cells produce and release CTLA-4, which typically inhibits anticancer responses.Cancer immunotherapy strategies have made it increasingly evident that the immune system plays an integral role in managing and destroying cancer. Nevertheless, many mechanisms of immune suppression exist that may inhibit antitumor immunity. Recently, strategies that implement antibodies directed against negative immunologic regulators have demonstrated significant success. Cytotoxic T-lymphocyte-associate protein-4 (CTLA-4) was the first immunologic checkpoint to be clinically targeted, by the cancer immunotherapeutic ipilimumab, an FDA-approved drug to treat melanoma. After T-cell activation, CTLA-4 is upregulated on the cell surface where it functions to downregulate T cell function. Ipilimumab binds to CTLA-4 on T cells, which blocks the inhibitory signals and enhances anti-cancer immune responses.
Immune checkpoints modulate either the activation or downplay of T cells but can be manipulated by cancer cells. We can strike back with newer drugs.