Candida albicans extracellular vesicles trigger type I IFN signalling via cGAS and STING.
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ABSTRACT:
SUBMITTER: Brown Harding H
PROVIDER: S-EPMC10959075 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Candida albicans extracellular vesicles trigger type I IFN signalling via cGAS and STING.
Brown Harding Hannah H Kwaku Geneva N GN Reardon Christopher M CM Khan Nida S NS Zamith-Miranda Daniel D Zarnowski Robert R Tam Jenny M JM Bohaen Collins K CK Richey Lauren L Mosallanejad Kenta K Crossen Arianne J AJ Reedy Jennifer L JL Ward Rebecca A RA Vargas-Blanco Diego A DA Basham Kyle J KJ Bhattacharyya Roby P RP Nett Jeniel E JE Mansour Michael K MK van de Veerdonk Frank L FL Kumar Vinod V Kagan Jonathan C JC Andes David R DR Nosanchuk Joshua D JD Vyas Jatin M JM
Nature microbiology 20240102 1
The host type I interferon (IFN) pathway is a major signature of inflammation induced by the human fungal pathogen, Candida albicans. However, the molecular mechanism for activating this pathway in the host defence against C. albicans remains unknown. Here we reveal that mice lacking cyclic GMP-AMP synthase (cGAS)-stimulator of IFN genes (STING) pathway components had improved survival following an intravenous challenge by C. albicans. Biofilm-associated C. albicans DNA packaged in extracellular ...[more]
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2022-04-04 | PXD030753 | Pride