| First Author | Carlyle JR | Year | 2004 |
| Journal | Proc Natl Acad Sci U S A | Volume | 101 |
| Issue | 10 | Pages | 3527-32 |
| PubMed ID | 14990792 | Mgi Jnum | J:89706 |
| Mgi Id | MGI:3041277 | Doi | 10.1073/pnas.0308304101 |
| Citation | Carlyle JR, et al. (2004) Missing self-recognition of Ocil/Clr-b by inhibitory NKR-P1 natural killer cell receptors. Proc Natl Acad Sci U S A 101(10):3527-32 |
| abstractText | The NKR-P1 family of C-type lectin-like receptors are expressed on natural killer (NK) cells and NKT cells. We report the cloning and characterization of a cognate ligand for the inhibitory mouse NK receptors (NKR)-P1B and NKR-P1D (CD161b/d). The NKR-P1B/D ligand is osteoclast inhibitory lectin (Ocil), also known as Clr-b, a member of a previously cloned group of C-type lectin-related (Clr) proteins linked to the NKR-P1 receptors in the mouse NK gene complex (NKC). Expression of Ocil/Clr-b on mouse tumor cell lines inhibits NK cell-mediated killing. Inhibition is blocked with a new mAb (4A6) specific for Ocil/Clr-b. By using 4A6 mAb, we demonstrate that Ocil/Clr-b is displayed at high levels on nearly all hematopoietic cells, with the exception of erythrocytes, in a pattern that is similar to that of class I MHC molecules. Remarkably, Ocil/Clr-b is frequently down-regulated on mouse tumor cell lines, indicating a role for this receptor-ligand system in a new form of 'missing self-recognition' of tumor cells. |
