Redundant role of TLR9 for anti-Candida host defense.
until further notice
SourceImmunobiology, 213, 8, (2008), pp. 613-620
Article / Letter to editor
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SubjectN4i 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 defense
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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