The sequential mechanisms of (1) CD47 activation by PKHB1, (2) exposure to several DAMPs by atypical caspase-independent and calcium-dependent signaling in cell death, (3) the enhanced maturation of bone marrow-derived DCs with proper antigen presentation, and (4) the stimulation of antitumor T cell responses in an in vivo L5178Y-R tumor model using syngeneic BALB/c mice, were obtained using PKHB1-TCLs. Here, CD47 is linked to neoplasm.