The Journal of Immunology · 2009 · 285 citations · 19 references
Life SciencesImmunologyMicrobiologyHost-pathogen InteractionsInnate ImmunityMicrobial PathogenesisFungal Cell BiologyFungal InfectionsFungal PathogenesisInflammasome ActivationInflammatory SignalingInnate Immune Signaling PathwaysCandida Albicans InfectionFilamentous FormHost Immune Response To CandidaInnate Cytokine ResponsesInnate Immune EffectorsMacrophage Inflammasome ActivationMacrophage-fungus InteractionsNlrp3 Inflammasome
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.
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Cryopyrin activates the inflammasome in response to toxins and ATP
Sanjeev Mariathasan, David S. Weiss, Kim Newton et al. · Nature · 2006 · 3K citations
Nonfilamentous C. albicans Mutants Are Avirulent
Hsiu‐Jung Lo, Julia R. Köhler, Beth DiDomenico et al. · Cell · 1997 · 1.8K citations · Full text