van de Veerdonk Frank Leo, Netea Mihai G, Jansen Trees J, Jacobs Liesbeth, Verschueren Ineke, van der Meer Jos W M, Kullberg Bart Jan
Immunobiology. 2008;213(8):613-20. doi: 10.1016/j.imbio.2008.05.002. Epub 2008 Jun 26.
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.
在播散性念珠菌病小鼠模型和人外周血单个核细胞(PBMC)中,研究了Toll样受体9(TLR9)在识别白色念珠菌和抗念珠菌宿主防御中的作用。用人类TLR9特异性抑制剂阻断TLR9或刺激从TLR9缺陷(TLR9-/-)小鼠分离的细胞,导致白色念珠菌诱导的细胞因子产生减少20%-30%。然而,这种缺陷并未伴随着TLR9-/-和TLR9+/+小鼠在死亡率和器官真菌生长方面的差异。总之,TLR9是白色念珠菌的病原体识别受体,TLR9参与了对白色念珠菌应答时细胞因子的诱导。然而,TLR9-/-小鼠中的细胞因子缺陷由替代途径补偿,并且在小鼠播散性念珠菌病模型中,TLR9依赖性途径似乎是多余的。