Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection.
Dectin-3 Is Not Required for Protection against Cryptococcus neoformans Infection.
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dectin-3不需要防御新甲壳虫感染。
DOI：
10.1371/journal.pone.0169347
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Wormley FL Jr
中科院分区：
文献类型：
--
作者：
Campuzano A;Castro-Lopez N;Wozniak KL;Leopold Wager CM;Wormley FL Jr
C型凝集素受体(CLR)是一种多种多样的跨膜蛋白，具有模式识别受体(PRR)的功能，是协调针对病原体的免疫反应所必需的。CLR已被证明在识别和保护真菌病原体方面发挥着重要作用。Dectin-3(也称为mc1、clecsf8或clec4d)是一种髓系细胞特异性CLR，识别存在于真菌病原体细胞壁中的分枝杆菌海藻糖6，6‘-二肌甘露糖(Tdm)和α-甘露聚糖。到目前为止，Dectin-3在调节对新生葡萄球菌的保护性免疫反应中的潜在作用尚未确定。因此，我们使用实验性的肺隐球菌病小鼠模型来评估Dectin-3缺乏对针对新生弧菌的保护性免疫反应的发展的影响。Dectin-3缺乏并不导致小鼠对实验性肺部新生葡萄球菌感染的易感性增加。此外，Dectin-3缺陷小鼠与野生型感染小鼠相比，在肺白细胞募集和细胞因子产生方面也没有显著差异。此外，我们没有观察到Dectin-3缺陷的树突状细胞和巨噬细胞的摄取和抗隐球菌活性的差异。总之，我们的研究表明Dectin-3对于介导对肺部新生芽孢杆菌感染的保护性免疫反应是必不可少的。
C-type lectin receptors (CLRs) are diverse, trans-membrane proteins that function as pattern recognition receptors (PRRs) which are necessary for orchestrating immune responses against pathogens. CLRs have been shown to play a major role in recognition and protection against fungal pathogens. Dectin-3 (also known as MCL, Clecsf8, or Clec4d) is a myeloid cell-specific CLR that recognizes mycobacterial trehalose 6,6’-dimycolate (TDM) as well as α-mannans present in the cell wall of fungal pathogens. To date, a potential role for Dectin-3 in the mediation of protective immune responses against C. neoformans has yet to be determined. Consequently, we evaluated the impact of Dectin-3 deficiency on the development of protective immune responses against C. neoformans using an experimental murine model of pulmonary cryptococcosis. Dectin-3 deficiency did not lead to increased susceptibility of mice to experimental pulmonary C. neoformans infection. Also, no significant differences in pulmonary leukocyte recruitment and cytokine production were observed in Dectin-3 deficient mice compared to wild type infected mice. In addition, we observed no differences in uptake and anti-cryptococcal activity of Dectin-3 deficient dendritic cells and macrophages. Altogether, our studies show that Dectin-3 is dispensable for mediating protective immune responses against pulmonary C. neoformans infection.