| First Author | Momota M | Year | 2020 |
| Journal | Int Immunol | Volume | 32 |
| Issue | 3 | Pages | 203-212 |
| PubMed ID | 31630209 | Mgi Jnum | J:289451 |
| Mgi Id | MGI:6394181 | Doi | 10.1093/intimm/dxz070 |
| Citation | Momota M, et al. (2020) ZBP1 governs the inflammasome-independent IL-1alpha and neutrophil inflammation that play a dual role in anti-influenza virus immunity. Int Immunol 32(3):203-212 |
| abstractText | Influenza A virus (IAV) triggers the infected lung to produce IL-1 and recruit neutrophils. Unlike IL-1beta, however, little is known about IL-1alpha in terms of its mechanism of induction, action and physiological relevance to the host immunity against IAV infection. In particular, whether Z-DNA-binding protein 1 (ZBP1), a key molecule for IAV-induced cell death, is involved in the IL-1alpha induction, neutrophil infiltration and the physiological outcome has not been elucidated. Here, we show in a murine model that the IAV-induced IL-1alpha is mediated solely by ZBP1, in an NLRP3-inflammasome-independent manner, and is required for the optimal IL-1beta production followed by the formation of neutrophil extracellular traps (NETs). During IAV infection, ZBP1 displays a dual role in anti-IAV immune responses mediated by neutrophils, resulting in either protective or pathological outcomes in vivo. Thus, ZBP1-mediated IL-1alpha production is the key initial step of IAV-infected NETs, regulating the duality of the consequent lung inflammation. |
