Cytokines in the host response to Candida vaginitis: Identifying a role for non-classical immune mediators, S100 alarmins.
Cytokines in the host response to Candida vaginitis: Identifying a role for non-classical immune mediators, S100 alarmins.
复制标题
DOI：
10.1016/j.cyto.2011.11.021
复制
发表时间：
2012-04
期刊：
影响因子：
3.8
通讯作者：
Fidel, Paul L., Jr.
中科院分区：
文献类型：
--
作者：
Yano, Junko;Noverr, Mairi C.;Fidel, Paul L., Jr.
外阴阴道念珠菌病（VVC），由白色念珠菌引起，影响了相当多的妇女在其生育年龄。二十多年的研究一直集中在与症状感染的易感性或耐药性相关的机制上。Th1型CD4+ T细胞和下游细胞因子应答的适应性免疫被认为是抵抗粘膜念珠菌感染的主要宿主防御机制。然而，许多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保护作用有限。Th17在VVC中的作用现在才开始深入研究，结果已经显示出重大争议。另一方面，一项临床活菌攻毒研究和一个已建立的动物模型表明，症状性疾病与多形核白细胞（PMN）的阴道浸润密切相关，但对阴道真菌负荷没有影响。随后的研究确定S100A8和S100A9 Alarmins是急性PMN反应的关键趋化介质。这些趋化危险信号似乎是由阴道上皮细胞分泌的相互作用和早期粘附的念珠菌。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性应答的结果，而不是涉及经典免疫细胞和适应性应答的细胞因子的针对念珠菌的假定免疫缺陷。
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.
登录
查看更多内容
影响因子：
11.8
作者：
Babula, O;Lazdane, G;Witkin, SS
通讯作者：
Witkin, SS
影响因子：
3.1
作者：
De Bernardis, Flavia;Lucciarini, Roberta;Santoni, Giorgio
通讯作者：
Santoni, Giorgio
影响因子：
37.8
作者：
Croce K;Gao H;Wang Y;Mooroka T;Sakuma M;Shi C;Sukhova GK;Packard RR;Hogg N;Libby P;Simon DI
通讯作者：
Simon DI
DOI：
10.1007/s11596-008-0423-z
发表时间：
2008-08-01
影响因子：
--
作者：
Chen, Shanjuan;Li, Shaohua;Li, Jiawen
通讯作者：
Li, Jiawen
DOI：
10.1084/jem.20080132
发表时间：
2008-09-29
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Cheng P;Corzo CA;Luetteke N;Yu B;Nagaraj S;Bui MM;Ortiz M;Nacken W;Sorg C;Vogl T;Roth J;Gabrilovich DI
通讯作者：
Gabrilovich DI