| First Author | Olsson MY | Year | 1995 |
| Journal | Proc Natl Acad Sci U S A | Volume | 92 |
| Issue | 5 | Pages | 1649-53 |
| PubMed ID | 7878033 | Mgi Jnum | J:23319 |
| Mgi Id | MGI:71079 | Doi | 10.1073/pnas.92.5.1649 |
| Citation | Olsson MY, et al. (1995) Altered phenotype and function of natural killer cells expressing the major histocompatibility complex receptor Ly-49 in mice transgenic for its ligand. Proc Natl Acad Sci U S A 92(5):1649-53 |
| abstractText | The Ly-49 molecule has been shown to interact with major histocompatibility complex (MHC) class I molecules, and the lytic function of Ly-49+ natural killer (NK) cells from C57BL/6 (H-2b) mice is inhibited by the recognition of H-2Dd on tumor target cells. Introduction of a Ly-49 ligand, H-2Dd, into C57BL/6 mice did not alter the percentage of Ly-49+ NK cells (13-18%), but it led to three functional effects on this subset. (i) The Ly-49 expression in the positive population was reduced by 30-50% compared to C57BL/6 control mice. (ii) While this Ly-49+ subset (Ly-49lo) in the transgenic mice failed to kill BALB/c concanavalin A (Con A) blasts, which have high H-2Dd expression, it was capable of killing SP2/0 tumor cells, which have low H-2Dd expression. Ly-49+ NK cells (Ly-49hi) from nontransgenic mice failed to kill both of these H-2Dd-expressing target cells. (iii) In the transgenic mice, the Ly-49+ subset acquired the ability to kill C57BL/6 Con A blasts, in contrast to the Ly-49+ NK cells of C57BL/6 mice. We propose a receptor-calibration hypothesis, where low receptor density on the effector cells imposed by selection or adaptation to the environment allows higher sensitivity for detection of reduced self-MHC ligands on potential target cells. |
