Defining the mechanisms of action of immune checkpoint blockade therapies is essential for effectively designing combination therapeutic approaches and developing the next generation of immunotherapies. In this issue, Schaafsma and colleagues report that V-domain immunoglobulin suppressor of T-cell activation antagonism acts through mechanisms distinct from anti-CTLA-4 and anti-programmed cell death protein 1 via remodeling of the myeloid-cell compartment and modulating T-cell quiescence. See related article by Schaafsma et al. p. 38 (1).
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