The secretory Candida effector Sce1 licenses fungal virulence by masking the immunogenicβ-1,3-glucan and promoting apoptosis of the host cells  

作　　者：Hongyu Wu Li Wang Wenjuan Wang Zhugui Shao Xin-Ming Jia Hui Xiao Jiangye Chen 

机构地区：[1]State Key Laboratory of Molecular Biology,Shanghai Institute of Biochemistry and Cell Biology,Center for Excellence in Molecular Cell Science,Chinese Academy of Sciences,University of Chinese Academy of Sciences,Shanghai,China [2]The Center for Microbes,Development and Health,Institut Pasteur of Shanghai,Chinese Academy of Sciences,University of Chinese Academy of Sciences,Shanghai,China [3]Clinical Medicine Scientific and Technical Innovation Center,Shanghai Tenth People's Hospital,Tongji University School of Medicine,Shanghai,China [4]Key Laboratory of Infection and Immunity of Shandong Province and Department of Immunology,School of Biomedical Sciences,Shandong University,Jinan,China

出　　处：《mLife》2023年第2期159-177,共19页微生物（英文）

基　　金：supported by the National Natural Science Foundation of China grants(31970144,81720108019,and 32030040);the National Key Research and Development Program of China(2021YFA1301400);the Shanghai Municipal Science and Technology Major Project(2019SHZDZX02).

摘　　要：Candida albicans deploys a variety of mechanisms such as morphological switch and elicitor release to promote virulence.However,the intricate interactions between the fungus and the host remain poorly understood,and a comprehensive inventory of fungal virulence factors has yet to be established.In this study,we identified a C.albicans secretory effector protein Sce1,whose induction and secretion are associated with vagina‐simulative conditions and chlamydospore formation.Sequence alignment showed that Sce1 belongs to a Pir family in C.albicans,which is conserved across several fungi and primarily characterized as aβ‐glucan binding protein in the Saccharomyces cerevisiae.Mechanically,Sce1 is primarily localized to the cell wall in a cleaved form as an alkali‐labileβ‐1,3‐glucan binding protein and plays a role in maskingβ‐glucan in acidic environments and chlamydospores,a feature that might underline C.albicans'ability to evade host immunity.Further,a cleaved short form of Sce1 protein could be released into extracellular compartments and presented in bone marrow‐derived macrophages infected with chlamydospores.This cleaved short form of Sce1 also demonstrated a unique ability to trigger the caspases‐8/9‐dependent apoptosis in various host cells.Correspondingly,genetic deletion of SCE1 led to dampened vaginal colonization of C.albicans and diminished fungal virulence during systemic infection.The discovery of Sce1 as a versatile virulence effector that executes at various compartments sheds light on the fungus–host interactions and C.albicans pathogenesis.

关 键 词：APOPTOSIS Candida albicans EFFECTOR immune evasion Β-GLUCAN 

分 类 号：Q93[生物学—微生物学]