Department of Microbiology, Immunology and Parasitology, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Cytokine. 2012 Apr;58(1):118-28. doi: 10.1016/j.cyto.2011.11.021. Epub 2011 Dec 17.
Vulvovaginal candidiasis (VVC), caused by Candida albicans, affects a significant number of women during their reproductive years. More than two decades of research have been focused on the mechanisms associated with susceptibility or resistance to symptomatic infection. Adaptive immunity by Th1-type CD4(+) T cells and downstream cytokine responses are considered the predominant host defense mechanisms against mucosal Candida infections. However, numerous clinical and animal studies have indicated no or limited protective role of cells and cytokines of the Th1 or Th2 lineage against vaginal infection. The role for Th17 is only now begun to be investigated in-depth for VVC with results already showing significant controversy. On the other hand, a clinical live-challenge study and an established animal model have shown that a symptomatic condition is intimately associated with the vaginal infiltration of polymorphonuclear leukocytes (PMNs) but with no effect on vaginal fungal burden. Subsequent studies identified S100A8 and S100A9 alarmins as key chemotactic mediators of the acute PMN response. These chemotactic danger signals appear to be secreted by vaginal epithelial cells upon interaction and early adherence of Candida. Thus, instead of a putative immunodeficiency against Candida involving classical immune cells and cytokines of the adaptive response, the pathological inflammation in VVC is now considered a consequence of a non-productive innate response initiated by non-classical immune mediators.
外阴阴道假丝酵母菌病（VVC），由白假丝酵母菌引起，在育龄妇女中发病率较高。二十多年来，人们一直致力于研究与症状性感染易感性或抵抗力相关的机制。Th1 型 CD4+T 细胞的适应性免疫和下游细胞因子反应被认为是针对黏膜假丝酵母菌感染的主要宿主防御机制。然而，大量的临床和动物研究表明，Th1 或 Th2 谱系的细胞和细胞因子对阴道感染没有保护作用或作用有限。Th17 细胞的作用仅在最近才开始深入研究 VVC，研究结果已经显示出显著的争议。另一方面，一项临床活体挑战研究和已建立的动物模型表明，一种症状与多形核白细胞（PMN）阴道浸润密切相关，但对阴道真菌负荷没有影响。随后的研究确定 S100A8 和 S100A9 警报素是急性 PMN 反应的关键趋化介质。这些趋化危险信号似乎是阴道上皮细胞在与假丝酵母菌相互作用和早期黏附时分泌的。因此，VVC 中的病理性炎症现在被认为是由非经典免疫介质引发的非生产性先天反应的结果，而不是针对假丝酵母菌的所谓适应性免疫细胞和细胞因子的免疫缺陷。
