Fig. 3.
Fig. 3. CFU-GM inhibition is abrogated by blocking antibody to HLA-A2.1, indicating MHC-I–restricted inhibition of targets. Day 20 PR1-pulsed CTL2 inhibit CFU-GM from P4 (CML-AP) by 89% compared to P4 cultured without CTL2 (P + .0006). CTL2 did not inhibit CFU-GM from the D4, the HLA-identical normal marrow donor to patient P4. There was no effect on CFU-GM when anti-HLA-A2.1 antibody is added to P4 alone; however, when antibody was added during the 4-hour incubation of CTL2 with P4 colony growth is restored by 66%. 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 is abrogated by blocking antibody to HLA-A2.1, indicating MHC-I–restricted inhibition of targets. Day 20 PR1-pulsed CTL2 inhibit CFU-GM from P4 (CML-AP) by 89% compared to P4 cultured without CTL2 (P + .0006). CTL2 did not inhibit CFU-GM from the D4, the HLA-identical normal marrow donor to patient P4. There was no effect on CFU-GM when anti-HLA-A2.1 antibody is added to P4 alone; however, when antibody was added during the 4-hour incubation of CTL2 with P4 colony growth is restored by 66%. 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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