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Significance Antibody blockade of the B7-H1/PD-1 interaction induces regression of advanced human cancers in some patients, while recurrence occurs in others due to tumor escape from T cell attack. Here, we describe a possible mechanism of tumor escape from therapy caused by biased stimulation of T cells to dominant antigen. Based on this finding, we tested a split immunization approach to prevent cancer recurrence in mouse tumor models. These findings may help design approaches for combination cancer immunotherapies.

B7-H1 maintains the polyclonal T cell response by protecting dendritic cells from cytotoxic T lymphocyte destruction