Expression of activating NK cell receptors after chronic stimulation
| Stimulator cell . | Cognate receptor . | NK cell receptor expression . | |||||
|---|---|---|---|---|---|---|---|
| NK1.1 . | NKG2D . | CD16 . | Ly49D . | Ly49H . | Nkp46 . | ||
| RMA* | Unknown | 100# | 100 100 | 100 | 100 | 100 | 100 |
| RMA H60† | NKG2D | 95 ± 13 | 18 ± 8** | 57 ± 14 | 93 ± 14 | 95 ± 23 | 92 ± 7 |
| RMA+αThy1‡ | CD16 | 89 ± 18 | 97 ± 14 | 51 ± 17 | 106 ± 20 | 100 ± 1 | ND†† |
| RMA/S§ | Unknown | 108 ± 8 | 122 ± 17 | 95 ± 14 | 100 ± 8 | 105 ± 7 | ND |
| CHO‖ | Ly49D | 64 ± 18 | 92 ± 38 | 66 ± 15 | 41 ± 10 | 85 ± 1 | ND |
| RMA m157¶ | Ly49H | ND | ND | ND | ND | ND | ND |
| Stimulator cell . | Cognate receptor . | NK cell receptor expression . | |||||
|---|---|---|---|---|---|---|---|
| NK1.1 . | NKG2D . | CD16 . | Ly49D . | Ly49H . | Nkp46 . | ||
| RMA* | Unknown | 100# | 100 100 | 100 | 100 | 100 | 100 |
| RMA H60† | NKG2D | 95 ± 13 | 18 ± 8** | 57 ± 14 | 93 ± 14 | 95 ± 23 | 92 ± 7 |
| RMA+αThy1‡ | CD16 | 89 ± 18 | 97 ± 14 | 51 ± 17 | 106 ± 20 | 100 ± 1 | ND†† |
| RMA/S§ | Unknown | 108 ± 8 | 122 ± 17 | 95 ± 14 | 100 ± 8 | 105 ± 7 | ND |
| CHO‖ | Ly49D | 64 ± 18 | 92 ± 38 | 66 ± 15 | 41 ± 10 | 85 ± 1 | ND |
| RMA m157¶ | Ly49H | ND | ND | ND | ND | ND | ND |
RMA cells activate NK cells through unknown activation receptors. Lysis is prevented by inhibitory Ly49 receptors specific for MHC class I molecules. Consequently, RMA cells are resistant to NK cell–mediated lysis.
Transfection of RMA cells with H60 overcomes MHC-I–dependent inhibition due to an excess of NK cell activation signals through NKG2D engagement.
Coating of RMA cells with anti-Thy1 mAb (αThy1) results in ADCC through CD16 engagement.
Like the parental RMA, RMA/S cells stimulate NK cells through unknown receptors. Lysis occurs since RMA/S express very low levels of MHC-I molecules such that NK cells are not inhibited. This is known as “missing-self recognition.”
The hamster MHC-I molecule Hm1-C4 expressed on CHO cells activates NK cells through Ly49D engagement.
Transfection of RMA cells with MCMV m157 overcomes MHC-I–dependent inhibition due to an excess of NK cell activation signals through Ly49H engagement.
The mean fluorescence intensity of staining of the indicated receptor in NK cells exposed to control RMA cells was arbitrarily set to 100.
Significant deviations from 100 are indicated in bold face.
nd indicates not determined.