A frameshift polymorphism in P2X5 elicits an allogeneic cytotoxic T lymphocyte response associated with remission of chronic myeloid leukemia
J. Clin. Invest. Björn de Rijke, et al. 115:3506 doi:10.1172/JCI24832 [Go to this article.]

Figure 1
Specific reactivity of HLA-B*0702–restricted CTL RP1 against hematopoietic cells. (A) Specific cytotoxicity was tested in ⁵¹Cr release assays against EBV-LCLs of the recipient (Rt) and donor (Do). NK-sensitive K562 cells were used to determine nonspecific lysis. Effector to target (E/T) ratios are indicated. (B) Production of IFN-γ by CTL RP1 stimulated with recipient EBV-LCLs, EBV-LCLs of 2 unrelated individuals (nos. 1 and 2) sharing HLA-B7 with the recipient, and an EBV-LCL of an HLA class I–mismatched individual (no. 3) that was transduced with HLA-B*0702. Data are displayed as mean IFN-γ release ± SD of triplicate wells. (C) Specific cytotoxicity against hematopoietic cells of lymphoid origin (EBV-LCLs, PHA-stimulated T cells, and CD40L-stimulated B cells) and BM-derived fibroblasts incubated with 10 ng/ml TNF-α and 100 U/ml IFN-γ for 2 days before ⁵¹Cr labeling. The E/T ratio was 1:1. (D) IFN-γ production by CTL RP1 upon stimulation with hematopoietic cells of myeloid origin (monocytes, immature DCs [iDC] and mature DCs [mDC]).