Candida albicans infection affords protection against reinfection via functional reprogramming of monocytes.

Cell Host Microbe
Authors
Keywords
Abstract

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 β-glucans induced functional reprogramming of monocytes, leading to enhanced cytokine production in vivo and in vitro. The training required the β-glucan receptor dectin-1 and the noncanonical Raf-1 pathway. Monocyte training by β-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.

Year of Publication
2012
Journal
Cell Host Microbe
Volume
12
Issue
2
Pages
223-32
Date Published
2012 Aug 16
ISSN
1934-6069
URL
DOI
10.1016/j.chom.2012.06.006
PubMed ID
22901542
PubMed Central ID
PMC3864037
Links
Grant list
P30 DK043351 / DK / NIDDK NIH HHS / United States
R01 AI062773 / AI / NIAID NIH HHS / United States
DK 83756 / DK / NIDDK NIH HHS / United States
AI 062773 / AI / NIAID NIH HHS / United States
DK 043351 / DK / NIDDK NIH HHS / United States
R01 DK083756 / DK / NIDDK NIH HHS / United States