| First Author | Wiemann K | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 2 | Pages | 720-9 |
| PubMed ID | 16002667 | Mgi Jnum | J:100675 |
| Mgi Id | MGI:3589294 | Doi | 10.4049/jimmunol.175.2.720 |
| Citation | Wiemann K, et al. (2005) Systemic NKG2D down-regulation impairs NK and CD8 T cell responses in vivo. J Immunol 175(2):720-9 |
| abstractText | The immunoreceptor NKG2D stimulates activation of cytotoxic lymphocytes upon engagement with MHC class I-related NKG2D ligands of which at least some are expressed inducibly upon exposure to carcinogens, cell stress, or viruses. In this study, we investigated consequences of a persistent NKG2D ligand expression in vivo by using transgenic mice expressing MHC class I chain-related protein A (MICA) under control of the H2-K(b) promoter. Although MICA functions as a potent activating ligand of mouse NKG2D, H2-K(b)-MICA mice appear healthy without aberrations in lymphocyte subsets. However, NKG2D-mediated cytotoxicity of H2-K(b)-MICA NK cells is severely impaired in vitro and in vivo. This deficiency concurs with a pronounced down-regulation of surface NKG2D that is also seen on activated CD8 T cells. As a consequence, H2-K(b)-MICA mice fail to reject MICA-expressing tumors and to mount normal CD8 T cell responses upon Listeria infection emphasizing the importance of NKG2D in immunity against tumors and intracellular infectious agents. |
