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Candida albicans induces monocyte training via epigenetic programming through a dectin 1-dependent pathway

GSE34260 Mus musculus; Homo sapiens Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing 15 samples Submitted 2012/12/21 Platform GPL9185Platform GPL9052
Summary
Non-specific protective effects against reinfection have been described following infection with Candida albicans. Here we show that mice defective in functional T and B lymphocytes were protected against reinfection with C. albicans in a monocyte-dependent manner. C. albicans and beta glucans induced functional programming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the beta glucan receptor dectin 1 and the non-canonical Raf 1 pathway. Monocyte training by beta-glucans was mediated by epigenetic mechanisms through genome-wide changes in histone trimethylation at H3K4. Pathway analysis showed specific induction of epigenetic changes in genes of innate immunity. The functional programming of monocytes, reminiscent of similar properties of NK cells, has been termed “trained immunity” and may be employed for the design of improved vaccination strategies.
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Also filed as BioProject PRJNA149747 and SRA study SRP009657. Searching any of these in the dataset finder brings you back here.

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