Fungal ligands released by innate immune effectors promote inflammasome activation during Aspergillus fumigatus infection.

ABSTRACT: Invasive pulmonary aspergillosis causes substantial mortality in immunocompromised individuals. Recognition of Aspergillus fumigatus by the host immune system leads to activation of the inflammasome, which provides protection against infection. However, regulation of inflammasome activation at the molecular level is poorly understood. Here, we describe two distinct pathways that coordinately control inflammasome activation during A. fumigatus infection. The C-type lectin receptor pathway activates both MAPK and NF-κB signalling, which leads to induction of downstream mediators, such as the transcription factor IRF1, and also primes the inflammasomes. Toll-like receptor signalling through the adaptor molecules MyD88 and TRIF in turn mediates efficient activation of IRF1, which induces IRGB1

SUBMITTER: Briard B 

PROVIDER: S-EPMC6619501 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature