| First Author | Joly S | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 6 | Pages | 3578-81 |
| PubMed ID | 19684085 | Mgi Jnum | J:152328 |
| Mgi Id | MGI:4358018 | Doi | 10.4049/jimmunol.0901323 |
| Citation | Joly S, et al. (2009) Cutting edge: Candida albicans hyphae formation triggers activation of the Nlrp3 inflammasome. J Immunol 183(6):3578-81 |
| abstractText | The proinflammatory cytokine IL-1beta plays an important role in antifungal immunity; however, the mechanisms by which fungal pathogens trigger IL-1beta secretion are unclear. In this study we show that infection with Candida albicans is sensed by the Nlrp3 inflammasome, resulting in the subsequent release of IL-1beta. The ability of C. albicans to switch from a unicellular yeast form into a filamentous form is essential for activation of the Nlrp3 inflammasome, as C. albicans mutants incapable of forming hyphae were defective in their ability to induce macrophage IL- 1beta secretion. Nlrp3-deficient mice also demonstrated increased susceptibility to infection with C. albicans, which is consistent with a key role for Nlrp3 in innate immune responses to the pathogen C. albicans. |
