Journal
CELL HOST & MICROBE
Volume 12, Issue 2, Pages 223-232Publisher
CELL PRESS
DOI: 10.1016/j.chom.2012.06.006
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Funding
- Vici Grant of the Netherlands Organization for Scientific Research
- Higher Education Commission of Pakistan
- Vidi Grant of the Netherlands Organization for Scientific Research
- All-Fun EU-FP7 grant
- DNA-in-action consortium
- Foundation for Fundamental Research on Matter (FOM)
- Netherlands Organisation for Scientific Research (NWO)
- US National Institutes of Health [AI 062773, DK 043351, DK 83756]
- Helmsley Trust
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Immunological memory in vertebrates is often exclusively attributed to T and B cell function. Recently it was proposed that the enhanced and sustained innate immune responses following initial infectious exposure may also afford protection against reinfection. Testing this concept of trained immunity, we show that mice lacking functional T and B lymphocytes are protected against reinfection with Candida albicans in a monocyte-dependent manner. C. albicans and fungal cell wall beta-glucans induced functional reprogramming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the beta-glucan receptor dectin-1 and the noncanonical Raf-1 pathway. Monocyte training by beta-glucans was associated with stable changes in histone trimethylation at H3K4, which suggests the involvement of epigenetic mechanisms in this phenomenon. The functional reprogramming of monocytes, reminiscent of similar NK cell properties, supports the concept of trained immunity and may be employed for the design of improved vaccination strategies.
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