Table 3.

Percentages of trisomy 8 cells in BMMC cultures after short-term culture




CD3d-BM + autologous Vβ-expanded CD8, %

MHC class 1 mAb, %

CD3d-BM + allogeneic CD8 cells, %
Patient
BM alone, no treatment, %
Direct cell contact
Separated by filter
Direct cell contact + Fas antagonist
mAb alone
mAb + autologous Vβ-expanded CD8
Matched
Mismatched
32   16   1   15   5   18   15   18   —  
15   35   4   30   14   22   28   29   —  
21
 
78
 
24
 
68
 
40
 
68
 
70
 
72
 
74
 



CD3d-BM + autologous Vβ-expanded CD8, %

MHC class 1 mAb, %

CD3d-BM + allogeneic CD8 cells, %
Patient
BM alone, no treatment, %
Direct cell contact
Separated by filter
Direct cell contact + Fas antagonist
mAb alone
mAb + autologous Vβ-expanded CD8
Matched
Mismatched
32   16   1   15   5   18   15   18   —  
15   35   4   30   14   22   28   29   —  
21
 
78
 
24
 
68
 
40
 
68
 
70
 
72
 
74
 

Samples were cocultured as described in “Patients, materials, and methods.” BM was T cell depleted using beads before cocultivation with lymphocytes or mAb. Purified expanded Vβ subfamilies were obtained by flow cytometric sorting. When lymphocytes were separated from BMMCs by a filter, the inhibitory effect of Vβ lymphocytes was not apparent, suggesting a dependence on direct cell-to-cell contact. Fas antagonist (1 μg/mL) partially blocked the effect of CD8 cells on trisomy 8, suggesting the importance of Fas-mediated apoptosis in the elimination of trisomy 8 cells. HLA class 1 mAb (1:20) also partially blocked the effect of expanded CD8 cells when it was incubated for 30 minutes with the lymphocyte-depleted BMMCs before the addition of lymphocytes. Allogeneic HLA class 1-mismatched CD8 cells, which would presumably be activated after cocultivation with BMMCs, did not decrease the proportion of trisomy 8 cells when they were added in 3-fold excess to autologous lymphocytes.

— indicates not done.

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