| First Author | Wang H | Year | 2015 |
| Journal | Cell Rep | Volume | 12 |
| Issue | 1 | Pages | 42-48 |
| PubMed ID | 26119741 | Mgi Jnum | J:224854 |
| Mgi Id | MGI:5689209 | Doi | 10.1016/j.celrep.2015.05.047 |
| Citation | Wang H, et al. (2015) Reciprocal Regulation between Enterovirus 71 and the NLRP3 Inflammasome. Cell Rep 12(1):42-8 |
| abstractText | Enterovirus 71 (EV71) is the major etiological agent of hand, foot, and mouth disease (HFMD). Early studies showed that EV71-infected patients with severe complications exhibited elevated plasma levels of IL-1beta, indicating that EV71 may activate inflammasomes. Our current study demonstrates that the NLRP3 inflammasome plays a protective role against EV71 infection of mice in vivo. EV71 replication in myeloid cells results in the activation of the NLRP3 inflammasome and secretion of IL-1beta. Conversely, EV71 counteracts inflammasome activation through cleavage of NLRP3 by viral proteases 2A and 3C, which cleave NLRP3 protein at the G493-L494 or Q225-G226 junction, respectively. Moreover, EV71 3C interacts with NLRP3 and inhibits IL-1beta secretion when expressed in mammalian cells. These results thus reveal a set of reciprocal regulations between enterovirus 71 and the NLRP3 inflammasome. |
