| First Author | Regunathan J | Year | 2005 |
| Journal | Blood | Volume | 105 |
| Issue | 1 | Pages | 233-40 |
| PubMed ID | 15328154 | Mgi Jnum | J:96378 |
| Mgi Id | MGI:3530375 | Doi | 10.1182/blood-2004-03-1075 |
| Citation | Regunathan J, et al. (2005) NKG2D receptor-mediated NK cell function is regulated by inhibitory Ly49 receptors. Blood 105(1):233-40 |
| abstractText | Interaction of the activating ligand H60 with NKG2D receptor constitutes a major stimulatory pathway for natural killer (NK) cells. The influence of inhibitory Ly49 receptors on NKG2D-mediated activation is not clearly understood. Here we show that the magnitude of NKG2D-mediated cytotoxicity is directly proportional to both the levels of H60 and the nature of major histocompatibility complex (MHC) class I molecules expressed on the target cells. The expression levels of H60 on the target cells determined the extent to which the inhibition by Ly49C/I receptors can be overridden. In contrast, even a higher expression of H60 molecule on the target cells failed to overcome the inhibition mediated by Ly49A/G receptors. Also, the level of interferon-gamma (IFN-gamma) and granulocyte-macrophage colony-stimulating factor (GM-CSF) generated by NK cells through anti-NKG2D monoclonal antibody (mAb)-mediated activation is significantly reduced by the presence of immobilized anti-Ly49A/G mAbs. Thus, NKG2D-mediated cytotoxicity and cytokine secretion results from the fine balance between activating and inhibitory receptors, thereby defining the NK cell-mediated immune responses. |
