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本文引用的文献

1
Complement plays a central role in Candida albicans-induced cytokine production by human PBMCs.补体在白念珠菌诱导人 PBMCs 产生细胞因子中发挥核心作用。
Eur J Immunol. 2012 Apr;42(4):993-1004. doi: 10.1002/eji.201142057.
2
Toll-like receptor 9 modulates macrophage antifungal effector function during innate recognition of Candida albicans and Saccharomyces cerevisiae.Toll 样受体 9 调节巨噬细胞抗真菌效应功能，在先天识别白念珠菌和酿酒酵母期间。
Infect Immun. 2011 Dec;79(12):4858-67. doi: 10.1128/IAI.05626-11. Epub 2011 Sep 26.
3
Candida albicans cell wall glycosylation may be indirectly required for activation of epithelial cell proinflammatory responses.白念珠菌细胞壁糖基化可能间接需要激活上皮细胞的促炎反应。
Infect Immun. 2011 Dec;79(12):4902-11. doi: 10.1128/IAI.05591-11. Epub 2011 Sep 19.
4
Next-generation computational genetic analysis: multiple complement alleles control survival after Candida albicans infection.下一代计算遗传分析：多种补体等位基因控制白色念珠菌感染后的存活。
Infect Immun. 2011 Nov;79(11):4472-9. doi: 10.1128/IAI.05666-11. Epub 2011 Aug 29.
5
STAT1 mutations in autosomal dominant chronic mucocutaneous candidiasis.常染色体显性遗传慢性黏膜皮肤念珠菌病中的 STAT1 突变。
N Engl J Med. 2011 Jul 7;365(1):54-61. doi: 10.1056/NEJMoa1100102. Epub 2011 Jun 29.
6
Vacuolar trafficking and Candida albicans pathogenesis.液泡运输与白色念珠菌致病机制
Commun Integr Biol. 2011 Mar;4(2):240-2. doi: 10.4161/cib.4.2.14717.
7
The dectin-1/inflammasome pathway is responsible for the induction of protective T-helper 17 responses that discriminate between yeasts and hyphae of Candida albicans.模式识别受体 dectin-1/炎症小体途径负责诱导保护性辅助性 T 细胞 17 反应，可区分白念珠菌的酵母相和菌丝相。
J Leukoc Biol. 2011 Aug;90(2):357-66. doi: 10.1189/jlb.1210702. Epub 2011 Apr 29.
8
IL-22 and TNF-α represent a key cytokine combination for epidermal integrity during infection with Candida albicans.IL-22 和 TNF-α 是感染白色念珠菌过程中维持表皮完整性的关键细胞因子组合。
Eur J Immunol. 2011 Jul;41(7):1894-901. doi: 10.1002/eji.201041197. Epub 2011 May 20.
9
Candida-host interactions in HIV disease: implications for oropharyngeal candidiasis.HIV疾病中念珠菌与宿主的相互作用：对口咽念珠菌病的影响。
Adv Dent Res. 2011 Apr;23(1):45-9. doi: 10.1177/0022034511399284.
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From attachment to damage: defined genes of Candida albicans mediate adhesion, invasion and damage during interaction with oral epithelial cells.从黏附到损伤：白念珠菌的明确基因在与口腔上皮细胞相互作用过程中介导黏附、侵袭和损伤。
PLoS One. 2011 Feb 23;6(2):e17046. doi: 10.1371/journal.pone.0017046.

白色念珠菌与哺乳动物固有宿主防御之间的相互作用。

Interplay between Candida albicans and the mammalian innate host defense.

机构信息

Department of Internal Medicine, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.

出版信息

Infect Immun. 2012 Apr;80(4):1304-13. doi: 10.1128/IAI.06146-11. Epub 2012 Jan 17.

DOI:10.1128/IAI.06146-11
PMID:22252867
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3318407/
Abstract

Candida albicans is both the most common fungal commensal microorganism in healthy individuals and the major fungal pathogen causing high mortality in at-risk populations, especially immunocompromised patients. In this review, we summarize the interplay between the host innate system and C. albicans, ranging from how the host recognizes, responds, and clears C. albicans infection to how C. albicans evades, dampens, and escapes from host innate immunity.

摘要

白色念珠菌既是健康个体中最常见的真菌共生微生物，也是导致高危人群（特别是免疫功能低下患者）高死亡率的主要真菌病原体。在这篇综述中，我们总结了宿主固有系统与白色念珠菌之间的相互作用，包括宿主如何识别、响应和清除白色念珠菌感染，以及白色念珠菌如何逃避、抑制和逃脱宿主固有免疫。