The mammalian Toll-like receptors (TLRs) are homologues of Drosophila Toll and constitute a novel protein family involved in the mediation of innate immunity and the activation of adaptive immunity. Analysis of infection with human pathogenic fungi Candida albicans and Aspergillus fumigatus implicated TLR2 and TLR4 in elicitation of immune responses. Cryptococcus neoformans is recognized by a process that uses TLR4. C. albicans induces immunostimulation through causative agents, such as mannan or its structural derivatives (e.g. phospholipomannan), which are recognized by the immune system as pathogen-associated molecular patterns and are located in the cell wall of fungi. Secreted aspartic proteinases represent a key virulence factor that contributes to the ability of C. albicans to cause mucosal and disseminated infections, and might be a further potential stimulator of TLRs. Simultaneous activation of other pattern recognition receptors collaborating with TLRs illustrates the cooperation of various chains within ligand-specific receptor complexes for the recognition of fungal pathogens and their cell wall components.

中文翻译：

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Toll样受体和先天性抗真菌反应。

哺乳动物的Toll样受体（TLR）是果蝇Toll的同源物，构成了一个新的蛋白质家族，参与先天免疫的介导和适应性免疫的激活。人类致病性真菌白色念珠菌和烟曲霉感染的分析涉及TLR2和TLR4引起的免疫反应。新型隐球菌是通过使用TLR4的过程识别的。白色念珠菌通过诸如甘露聚糖或其结构衍生物（例如磷脂酰甘露聚糖）等病原体诱导免疫刺激，这些病原体被免疫系统识别为病原体相关的分子模式，并位于真菌的细胞壁中。分泌的天冬氨酸蛋白酶代表关键的毒力因子，有助于白色念珠菌引起粘膜和弥散性感染，并可能进一步刺激TLR。与TLRs合作的其他模式识别受体的同时激活说明了配体特异性受体复合物中各种链的协同作用，以识别真菌病原体及其细胞壁成分。