Candida albicans Infection Affords Protection against Reinfection via Functional Reprogramming of Monocytes.
SourceCell Host & Microbe, 12, 2, (2012), pp. 223-232
Article / Letter to editor
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Cell Biology (UMC)
Cell Host & Microbe
SubjectIGMD 5: Health aging / healthy living N4i 1: Pathogenesis and modulation of inflammation; Molecular Biology; N4i 1: Pathogenesis and modulation of inflammation NCMLS 1: Infection and autoimmunity; N4i 2: Invasive mycoses and compromised host NCMLS 1: Infection and autoimmunity; NCMLS 6: Genetics and epigenetic pathways of disease
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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