美国贝勒医学院David B. Corry团队发现，白念珠菌通过血小板介导的T辅助2和T辅助17细胞极化引起保护性过敏反应。2021年9月9日，国际知名学术期刊《免疫》在线发表了这一成果。

研究人员用野生型和突变型白色念珠菌来确定了，这种常见的真菌是如何在小鼠中引起特征性的Th2和Th17细胞依赖的过敏性气道疾病。结果证明，白念珠菌不是通过作为霉菌基本毒力因素的蛋白酶，而是通过肽毒素念珠菌素（candidalysin）促进过敏性气道疾病。念珠菌素通过Von Willebrand因子（VWF）受体GB1α激活血小板，释放Wnt拮抗因子Dickkopf-1（Dkk-1）来驱动Th2和Th17细胞反应，并与肺部真菌负担减少相关。

血小板同时排除了由肺部真菌入侵导致的致命肺出血。因此，除了止血外，血小板还通过涉及念珠菌素、GFP1α和Dkk-1的抗真菌途径促进Th2和Th17反应，进而促进对白念珠菌气道霉菌病的保护。

据介绍，真菌气道感染（气道霉菌病）是过敏性气道疾病（如哮喘）的一个重要原因，但对真菌引发哮喘反应的机制却知之甚少。

附：英文原文

Title: Candida albicans elicits protective allergic responses via platelet mediated T helper 2 and T helper 17 cell polarization

Author: Yifan Wu, Zhimin Zeng, Yubiao Guo, Lizhen Song, Jill E. Weatherhead, Xinyan Huang, Yuying Zeng, Lynn Bimler, Cheng-Yen Chang, John M. Knight, Christian Valladolid, Hua Sun, Miguel A. Cruz, Bernhard Hube, Julian R. Naglik, Amber U. Luong, Farrah Kheradmand, David B. Corry

Issue&Volume: 2021-09-09

Abstract: Fungal airway infection (airway mycosis) is an important cause of allergic airwaydiseases such as asthma, but the mechanisms by which fungi trigger asthmatic reactionsare poorly understood. Here, we leverage wild-type and mutant Candida albicans to determine how this common fungus elicits characteristic Th2 and Th17 cell-dependentallergic airway disease in mice. We demonstrate that rather than proteinases thatare essential virulence factors for molds, C. albicans instead promoted allergic airway disease through the peptide toxin candidalysin.Candidalysin activated platelets through the Von Willebrand factor (VWF) receptorGP1bα to release the Wnt antagonist Dickkopf-1 (Dkk-1) to drive Th2 and Th17 cellresponses that correlated with reduced lung fungal burdens. Platelets simultaneouslyprecluded lethal pulmonary hemorrhage resulting from fungal lung invasion. Thus, inaddition to hemostasis, platelets promoted protection against C. albicans airway mycosis through an antifungal pathway involving candidalysin, GP1bα, and Dkk-1that promotes Th2 and Th17 responses.

DOI: 10.1016/j.immuni.2021.08.009

Source: https://www.cell.com/immunity/fulltext/S1074-7613(21)00339-3