Figure 5
Figure 5. H-2 inhibits NKG2D-dependent NK-cell activation. (A) Expression of NKG2D ligands on lymphoblasts from (BALB/c × C.B10) F1 and BALB/c mice. (B) Enriched NK cells from CB6F1 were cocultured with (BALB/c × C.B10) F1 lymphoblasts in the presence of combinations of blocking antibodies (saturating concentrations) to H-2Kd, H-2Dd, and NKG2D in the presence of anti-CD107a to detect degranulation. *Anti–H-2Kb group is significantly less than either anti–H-2Dd or combo group (P < .002), but there is no significant difference between the anti–H-2Dd versus the combo group. **Anti-NKG2D + anti–H-2Dd group is significantly greater than anti–H-2Kb + anti-NKG2D (P < .0005), but significantly less than MHC class I blocking groups; P = .04 for anti–H-2Kb alone. Bar graphs of results shown are 1 representative experiment of 3 independent experiments performed. Error bars represent SEM.

H-2 inhibits NKG2D-dependent NK-cell activation. (A) Expression of NKG2D ligands on lymphoblasts from (BALB/c × C.B10) F1 and BALB/c mice. (B) Enriched NK cells from CB6F1 were cocultured with (BALB/c × C.B10) F1 lymphoblasts in the presence of combinations of blocking antibodies (saturating concentrations) to H-2Kd, H-2Dd, and NKG2D in the presence of anti-CD107a to detect degranulation. *Anti–H-2Kb group is significantly less than either anti–H-2Dd or combo group (P < .002), but there is no significant difference between the anti–H-2Dd versus the combo group. **Anti-NKG2D + anti–H-2Dd group is significantly greater than anti–H-2Kb + anti-NKG2D (P < .0005), but significantly less than MHC class I blocking groups; P = .04 for anti–H-2Kb alone. Bar graphs of results shown are 1 representative experiment of 3 independent experiments performed. Error bars represent SEM.

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