| First Author | Kupz A | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 5 | Pages | e97418 |
| PubMed ID | 24827856 | Mgi Jnum | J:217355 |
| Mgi Id | MGI:5613786 | Doi | 10.1371/journal.pone.0097418 |
| Citation | Kupz A, et al. (2014) In vivo IFN-gamma secretion by NK cells in response to Salmonella typhimurium requires NLRC4 inflammasomes. PLoS One 9(5):e97418 |
| abstractText | Natural killer (NK) cells are a critical part of the innate immune defense against viral infections and for the control of tumors. Much less is known about how NK cells contribute to anti-bacterial immunity. NK cell-produced interferon gamma (IFN-gamma) contributes to the control of early exponential replication of bacterial pathogens, however the regulation of these events remains poorly resolved. Using a mouse model of invasive Salmonellosis, here we report that the activation of the intracellular danger sensor NLRC4 by Salmonella-derived flagellin within CD11c+ cells regulates early IFN-gamma secretion by NK cells through the provision of interleukin 18 (IL-18), independently of Toll-like receptor (TLR)-signaling. Although IL18-signalling deficient NK cells improved host protection during S. Typhimurium infection, this increased resistance was inferior to that provided by wild-type NK cells. These findings suggest that although NLRC4 inflammasome-driven secretion of IL18 serves as a potent activator of NK cell mediated IFN-gamma secretion, IL18-independent NK cell-mediated mechanisms of IFN-gamma secretion contribute to in vivo control of Salmonella replication. |
