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Publication year
2008Source
Immunobiology, 213, 8, (2008), pp. 613-20ISSN
Publication type
Article / Letter to editor
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Organization
Internal Medicine
Journal title
Immunobiology
Volume
vol. 213
Issue
iss. 8
Page start
p. 613
Page end
p. 20
Subject
N4i 1: Pathogenesis and modulation of inflammation; N4i 2: Invasive mycoses and compromised host; NCMLS 1: Immunity, infection and tissue repair; NCMLS 1: Infection and autoimmunity; UMCN 4.1: Microbial pathogenesis and host defenseAbstract
The role of Toll-like receptor-9 (TLR9) in the recognition of Candida albicans and anti-Candida host defense was investigated in a murine model of disseminated candidiasis and in human peripheral blood mononuclear cells (PBMC). Blocking TLR9 by a specific inhibitor of human TLR9 or stimulation of cells isolated from TLR9-deficient (TLR9-/-) mice resulted in a 20-30% reduction in cytokine production induced by C. albicans. However, this defect was not accompanied by differences in mortality and organ fungal growth between TLR9-/- and TLR9+/+ mice. In conclusion, TLR9 is a pathogen-recognition receptor for C. albicans, and TLR9 is involved in the induction of cytokines in response to C. albicans. However, the cytokine defect in TLR9-/- mice is compensated by alternative pathways, and the TLR9-dependent pathway seems to be redundant in the disseminated candidiasis model in mice.
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- Academic publications [238441]
- Electronic publications [122508]
- Faculty of Medical Sciences [90373]
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