| First Author | Mason LH | Year | 1994 |
| Journal | J Leukoc Biol | Volume | 55 |
| Issue | 3 | Pages | 362-70 |
| PubMed ID | 7509843 | Mgi Jnum | J:17053 |
| Mgi Id | MGI:65108 | Doi | 10.1002/jlb.55.3.362 |
| Citation | Mason LH, et al. (1994) LGL-1: a potential triggering molecule on murine NK cells. J Leukoc Biol 55(3):362-70 |
| abstractText | Natural killer (NK) cells mediate non-major histocompatibility complex-restricted lysis of tumor cells, lymphokine-activated killing (LAK), antibody-dependent cellular cytotoxicity (ADCC), and reverse ADCC (RADCC). LGL-1+ cells identify a major subset (50%) of murine NK cells. Here we demonstrate that monoclonal antibodies (mAbs) to LGL-1 consistently induce interleukin-2-cultured, and Corynebacterium parvum (in vivo)-activated NK cells to induce RADCC. LGL-1 triggering of activated NK cells coincides with enhanced LGL-1 expression. Testing of murine mAbs to epitopes of CD2 only appears to augment RADCC induced by mAb NK-1.1 on fresh NK cells. Immunoprecipitation of the LGL-1 antigen reveals a highly disulfide-linked 40-kDa homodimer subunit that is N-glycosylated. Therefore, LGL-1 may be similar to other recently characterized NK-associated antigens such as NK-1.1, Ly-49, and NKR-PI. We conclude that although LGL-1 is expressed on resting NK cells, enhanced surface expression following activation is usually required for it to act as a signaling molecule. |
