Earlier quoted context omitted.
This method is not targeting mutations important for cancer, this is targeting "passenger" somatic mutations. You can't use this mechanism to target important mutations because only a minority of patients are going to be able to present an oncogenic mutation (e.g. BRAF V600E) as an antigen (because of differing HLA types). In those rare cases perhaps this therapy might succeed, although the tumor probably still has w…
I was under the impression that the major reason for the failure of current immunotherapy treatments is due to non-response, not excessive autoimmunity.
Sorry, you're absolutely right. I should say 'many', not 'most', my comment was hasty. It varies with the therapy and only a minority of patients fail because of adverse immune events, and the drug matters - ipilimumab (anti-CLTA4) had 10-15% severe immune-related adverse events, whereas anti-PD1 is much better tolerated (probably because the immune checkpoint is later). Combination therapies (ipi + nivo) have much higher adverse event rates, unsurprisingly.