| First Author | Di A | Year | 2018 |
| Journal | Immunity | Volume | 49 |
| Issue | 1 | Pages | 56-65.e4 |
| PubMed ID | 29958799 | Mgi Jnum | J:278146 |
| Mgi Id | MGI:6284483 | Doi | 10.1016/j.immuni.2018.04.032 |
| Citation | Di A, et al. (2018) The TWIK2 Potassium Efflux Channel in Macrophages Mediates NLRP3 Inflammasome-Induced Inflammation. Immunity 49(1):56-65.e4 |
| abstractText | Potassium (K(+)) efflux across the plasma membrane is thought to be an essential mechanism for ATP-induced NLRP3 inflammasome activation, yet the identity of the efflux channel has remained elusive. Here we identified the two-pore domain K(+) channel (K2P) TWIK2 as the K(+) efflux channel triggering NLRP3 inflammasome activation. Deletion of Kcnk6 (encoding TWIK2) prevented NLRP3 activation in macrophages and suppressed sepsis-induced lung inflammation. Adoptive transfer of Kcnk6(-/-) macrophages into mouse airways after macrophage depletion also prevented inflammatory lung injury. The K(+) efflux channel TWIK2 in macrophages has a fundamental role in activating the NLRP3 inflammasome and consequently mediates inflammation, pointing to TWIK2 as a potential target for anti-inflammatory therapies. |
