Oncology meets immunology: the cancer-immunity cycle.

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Expansion and activation of CD103+ dendritic cell progenitors at the tumor site enhances tumor responses to therapeutic PD-L1 and BRAF inhibition (2016, neutral): “The low numbers of CD8+ T cells present in B16 and Braf- mutant tumors and their limited accumulation upon BRAF and/ or PD-L1 blockade might explain the reduced clinical response to these treatments, as previously suggested (Chen and Mell- man, 2013; Gajewski et al., 2013).”
Type 1 diabetes (2002, neutral): “Immunotherapy trials in cancer have shown that agents reversing effector T cell exhaustion to increase antitumor immunity result in marked clinical responses ( 40 ).”
Targeting tumor-associated macrophages with anti-CSF-1R antibody reveals a strategy for cancer therapy. (2014, background): “Taken together, these observations provide rationale for future testing of combinations of RG7155 with currently available immunostimulatory therapies, such as sipuleucel-T and anti-CTLA-4 (Chen and Mellman 2013).”