Ashman R B, Papadimitriou J M
Department of Pathology, University of Western Australia, Nedlands, Australia.
Microbiol Rev. 1995 Dec;59(4):646-72. doi: 10.1128/mr.59.4.646-672.1995.
Host resistance against infections caused by the yeast Candida albicans is mediated predominantly by polymorphonuclear leukocytes and macrophages. Antigens of Candida stimulate lymphocyte proliferation and cytokine synthesis, and in both humans and mice, these cytokines enhance the candidacidal functions of the phagocytic cells. In systemic candidiasis in mice, cytokine production has been found to be a function of the CD4+ T helper (Th) cells. The Th1 subset of these cells, characterized by the production of gamma interferon and interleukin-2, is associated with macrophage activation and enhanced resistance against reinfection, whereas the Th2 subset, which produces interleukins-4, -6, and -10, is linked to the development of chronic disease. However, other models have generated divergent data. Mucosal infection generally elicits Th1-type cytokine responses and protection from systemic challenge, and identification of cytokine mRNA present in infected tissues of mice that develop mild or severe lesions does not show pure Th1- or Th2-type responses. Furthermore, antigens of C. albicans, mannan in particular, can induce suppressor cells that modulate both specific and nonspecific cellular and humoral immune responses, and there is an emerging body of evidence that molecular mimicry may affect the efficiency of anti-Candida responses within defined genetic contexts.
宿主对白色念珠菌感染的抵抗力主要由多形核白细胞和巨噬细胞介导。念珠菌抗原刺激淋巴细胞增殖和细胞因子合成，在人类和小鼠中，这些细胞因子增强吞噬细胞的杀念珠菌功能。在小鼠全身性念珠菌病中，已发现细胞因子的产生是CD4 + T辅助（Th）细胞的功能。这些细胞的Th1亚群以产生γ干扰素和白细胞介素-2为特征，与巨噬细胞活化和增强的抗再感染抵抗力相关，而产生白细胞介素-4、-6和-10的Th2亚群则与慢性病的发展有关。然而，其他模型产生了不同的数据。粘膜感染通常引发Th1型细胞因子反应并提供针对全身性攻击的保护，并且对发生轻度或重度病变的小鼠感染组织中存在的细胞因子mRNA的鉴定并未显示出纯Th1或Th2型反应。此外，白色念珠菌的抗原，特别是甘露聚糖，可以诱导调节特异性和非特异性细胞及体液免疫反应的抑制细胞，并且有新的证据表明分子模拟可能在特定遗传背景下影响抗念珠菌反应的效率。
