Dectin-1 is required for host defense against Pneumocystis carinii but not against Candida albicans
Dectin-1 is required for host defense against Pneumocystis carinii but not against Candida albicans
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DOI：
10.1038/ni1425
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发表时间：
2007-01-01
影响因子：
30.5
通讯作者：
Iwakura, Yoichiro
中科院分区：
文献类型：
--
作者：
Saijo, Shinobu;Fujikado, Noriyuki;Iwakura, Yoichiro
Dectin-1是一种C型凝集素，参与识别真菌细胞壁中发现的β-葡聚糖。我们产生了dectin-1缺陷小鼠，以确定dectin-1在防御病原性真菌中的重要性。在体外，β-葡聚糖诱导的野生型树突细胞和巨噬细胞产生的细胞因子在dectin-1缺陷纯合子细胞（“dectin-1敲除”细胞）中消失。在体内，dectin-1基因敲除小鼠比野生型小鼠更容易感染肺孢子虫，即使它们的细胞因子产生是正常的。然而，肺孢子虫感染的dectin-1基因敲除的巨噬细胞确实显示出活性氧的产生缺陷。与这些结果相反，野生型和dectin-1基因敲除小鼠对念珠菌感染同样敏感。因此，dectin-1是对某些真菌感染的免疫应答所必需的，因为对肺孢子虫的保护性免疫需要dectin-1来产生抗真菌活性氧，而对念珠菌则不需要。
Dectin-1 is a C-type lectin involved in the recognition of beta-glucans found in the cell walls of fungi. We generated dectin-1-deficient mice to determine the importance of dectin-1 in the defense against pathogenic fungi. In vitro, beta-glucan-induced cytokine production from wild-type dendritic cells and macrophages was abolished in cells homozygous for dectin-1 deficiency ('dectin-1-knockout' cells). In vivo, dectin-1-knockout mice were more susceptible than wild-type mice to pneumocystis infection, even though their cytokine production was normal. However, pneumocystis-infected dectin-1-knockout macrophages did show defective production of reactive oxygen species. In contrast to those results, wild-type and dectin-1-knockout mice were equally susceptible to candida infection. Thus, dectin-1 is required for immune responses to some fungal infections, as protective immunity to pneumocystis, but not to candida, required dectin-1 for the production of antifungal reactive oxygen species.