| First Author | Freund-Brown J | Year | 2017 |
| Journal | J Immunol | PubMed ID | 28794231 |
| Mgi Jnum | J:254737 | Mgi Id | MGI:6103677 |
| Doi | 10.4049/jimmunol.1700340 | Citation | Freund-Brown J, et al. (2017) Cutting Edge: Murine NK Cells Degranulate and Retain Cytotoxic Function without Store-Operated Calcium Entry. J Immunol |
| abstractText | Sustained Ca(2+) signaling, known as store-operated calcium entry (SOCE), occurs downstream of immunoreceptor engagement and is critical for cytotoxic lymphocyte signaling and effector function. CD8(+) T cells require sustained Ca(2+) signaling for inflammatory cytokine production and the killing of target cells; however, much less is known about its role in NK cells. In this study, we use mice deficient in stromal interacting molecules 1 and 2, which are required for SOCE, to examine the contribution of sustained Ca(2+) signaling to murine NK cell function. Surprisingly, we found that, although SOCE is required for NK cell IFN-gamma production in an NFAT-dependent manner, NK cell degranulation/cytotoxicity and tumor rejection in vivo remained intact in the absence of sustained Ca(2+) signaling. Our data suggest that mouse NK cells use different signaling mechanisms for cytotoxicity compared with other cytotoxic lymphocytes. |
