| Summary: | 碩士 === 長庚大學 === 生物醫學研究所 === 100 === G protein-coupled receptor 56 (GPR56) was discovered to be expressed abundantly in CD56dull CD16+ natural killer (NK) cells and its expression was down-regulated following exposure of NK cells to inflammatory cytokines. However, the role of GPR56 in NK cell function has yet to be clarified. Herein, connections among changes in GPR56 expression and associated typical NK characteristics including migration and cytotoxicity were investigated in NK-92 and human primary NK cells. In this study, we have successfully generated a stable clone of GPR56-expressing NK-92 cell line by retroviral infection as a primary NK-like model. Additionally, we also found that PMA treatment dramatically decreased the surface level of GPR56 by internalization but not shedding. Strikingly, over-expression of GPR56 significantly reduced the migration capacity of NK-92 when CXCL11 (I-TAC) or CXCL12 (SDF-1α) was used as chemoattractants. Moreover, cross-linking of monoclonal GPR56 antibody we generated was able to enhance the migration ability of GPR56-expressing NK-92 cells as well as human primary NK cells. Finally, our data revealed that GPR56 expression were not correlated with NK cytolytic ability. These results indicate that GPR56 might play a role in modulating NK motility.
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