| First Author | Zhu Q | Year | 2018 |
| Journal | Cell Rep | Volume | 22 |
| Issue | 12 | Pages | 3168-3174 |
| PubMed ID | 29562174 | Mgi Jnum | J:271039 |
| Mgi Id | MGI:6278380 | Doi | 10.1016/j.celrep.2018.02.096 |
| Citation | Zhu Q, et al. (2018) Detrimental Type I Interferon Signaling Dominates Protective AIM2 Inflammasome Responses during Francisella novicida Infection. Cell Rep 22(12):3168-3174 |
| abstractText | Interferons (IFNs) and inflammasomes are essential mediators of anti-microbial immunity. Type I IFN signaling drives activation of the AIM2 inflammasome in macrophages; however, the relative contribution of IFNs and inflammasome responses in host defense is less understood. We report intact AIM2 inflammasome responses in mice lacking type I IFN signaling during infection with F. novicida. Lack of type I IFN signaling conferred protection to F. novicida infection in contrast to the increased susceptibility in AIM2-deficient mice. Mice lacking both AIM2 and IFNAR2 were protected against the infection. The detrimental effects of type I IFN signaling were due to its ability to induce activation of apoptotic caspases and cell death. These results demonstrate the contrasting effects of type I IFN signaling and AIM2 during F. novicida infection in vivo and indicate a dominant role for type I IFNs in mediating detrimental responses despite the protective AIM2 inflammasome responses. |
