Fig. 1.
Fig. 1. CFU-GM inhibition by PR1-specific CTL1 against marrow from patients with CML or their HLA identical normal donors. Day 13 PR1-pulsed CTL1 inhibit CFU-GM from P1 (CML-CP) by 34% compared to P1 cultured without CTL1 (P = .006). Similarly, day 13 PR1-pulsed CTL1 inhibit CFU-GM from P2 (CML-BC) by 63% compared with P2 cells cultured in the absence of CTL1 (P = .007). CTL1 did not inhibit CFU-GM from the HLA-identical normal marrow donors, D1 and D2, to patients P1 and P2, respectively. Effectors were incubated with target cells at E:T ratio of 5:1 for 4 hours at 37°C before plating in methylcellulose, and colonies were counted on day 14 of culture. Three replicate wells were used to determine CFU-GM and data are displayed as mean colony counts ± standard deviation.

CFU-GM inhibition by PR1-specific CTL1 against marrow from patients with CML or their HLA identical normal donors. Day 13 PR1-pulsed CTL1 inhibit CFU-GM from P1 (CML-CP) by 34% compared to P1 cultured without CTL1 (P = .006). Similarly, day 13 PR1-pulsed CTL1 inhibit CFU-GM from P2 (CML-BC) by 63% compared with P2 cells cultured in the absence of CTL1 (P = .007). CTL1 did not inhibit CFU-GM from the HLA-identical normal marrow donors, D1 and D2, to patients P1 and P2, respectively. Effectors were incubated with target cells at E:T ratio of 5:1 for 4 hours at 37°C before plating in methylcellulose, and colonies were counted on day 14 of culture. Three replicate wells were used to determine CFU-GM and data are displayed as mean colony counts ± standard deviation.

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