Resistance to immune checkpoint blockade (ICB), a subject of increasing interest and relevance in the current cancer treatment landscape, is likely induced by several different and incompletely understood mechanisms, including host T-cell dysfunction/exhaustion, T-cell exclusion from the tumor microenvironment, and tumor-specific changes that dampen the antitumor immune response. In this issue, Kawase and colleagues examine tumor-specific changes that might contribute to anti-PD-1 resistance with a particular focus on reduced MHC class I expression as a potential mechanism of innate and acquired resistance to ICB. See related article by Kawase et al., p. 895 (1).
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