| First Author | Fernandes-Alnemri T | Year | 2010 |
| Journal | Nat Immunol | Volume | 11 |
| Issue | 5 | Pages | 385-93 |
| PubMed ID | 20351693 | Mgi Jnum | J:158968 |
| Mgi Id | MGI:4440997 | Doi | 10.1038/ni.1859 |
| Citation | Fernandes-Alnemri T, et al. (2010) The AIM2 inflammasome is critical for innate immunity to Francisella tularensis. Nat Immunol 11(5):385-93 |
| abstractText | Francisella tularensis, the causative agent of tularemia, infects host macrophages, which triggers production of the proinflammatory cytokines interleukin 1beta (IL-1beta) and IL-18. We elucidate here how host macrophages recognize F. tularensis and elicit this proinflammatory response. Using mice deficient in the DNA-sensing inflammasome component AIM2, we demonstrate here that AIM2 is required for sensing F. tularensis. AIM2-deficient mice were extremely susceptible to F. tularensis infection, with greater mortality and bacterial burden than that of wild-type mice. Caspase-1 activation, IL-1beta secretion and cell death were absent in Aim2(-/-) macrophages in response to F. tularensis infection or the presence of cytoplasmic DNA. Our study identifies AIM2 as a crucial sensor of F. tularensis infection and provides genetic proof of its critical role in host innate immunity to intracellular pathogens. |
