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Immune checkpoint blockade (ICB) therapies, such as the ones targeting cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) or programmed cell death protein 1 (PD-1), have displayed durable clinical responses in various cancers and are now approved by the FDA for a growing list of cancer types (1). Although these new immunotherapies have had a notable effect on cancer treatment, multiple mechanisms of immune resistance have been described. Tumors considered immunologically “cold”, with reduced or even absent infiltration of T-cells, are a major hurdle in the cancer immunotherapy field, and strategies to overcome this resistance mechanism constitute an unmet need. Recent efforts have focused on combining this immunotherapy approach with other therapies to maximize its potential. However, the candidate for these combination therapies are numerous and therefore the need for mechanism based and rationally designed therapies is needed.
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Campesato et al. (2017) studied this question.
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