| First Author | Corral L | Year | 2000 |
| Journal | Eur J Immunol | Volume | 30 |
| Issue | 3 | Pages | 920-30 |
| PubMed ID | 10741410 | Mgi Jnum | J:60892 |
| Mgi Id | MGI:1354060 | Doi | 10.1002/1521-4141(200003)30:3<920::AID-IMMU920>3.0.CO;2-P |
| Citation | Corral L, et al. (2000) NK cell expression of the killer cell lectin-like receptor G1 (KLRG1), the mouse homolog of MAFA, is modulated by MHC class I molecules. Eur J Immunol 30(3):920-30 |
| abstractText | Using a new mAb, 2F1, we characterize a mouse natural killer (NK) cell antigen termed 'killer cell lectin-like receptor G1' (KLRG1; formerly mouse MAFA or 2F1-Ag). KLRG1 is expressed on 30-60% of murine NK cells, and a small fraction of T cells, and is composed of a homodimer of glycosylated 30-38-kDa subunits. Strikingly, cell surface expression of KLRG1 by NK cells was substantially down-regulated in mice deficient for expression of class I molecules, in contrast to the Ly49 lectin-like NK receptors, which are up-regulated in class I-deficient mice. We could not demonstrate binding of KLRG1 to class I molecules in a cell-cell adhesion assay. Transgenic expression of KLRG1 under heterologous transcription elements was unaffected by class I deficiency, indicating that class I molecules do not affect the KLRG1 protein directly, and suggesting that regulation is at the level of expression of the endogenous KLRG1 gene. Evidence is presented that class I molecules regulate KLRG1 via interactions with class I-specific inhibitory Ly49 molecules and SHP-1 signaling. Thus, although KLRG1 and Ly49 molecules are both lectin-like inhibitory receptors that are regulated by class I expression, the effects of class I on the cell surface expression of the molecules are opposing, and the underlying regulatory mechanisms are distinct. |
