Saunus Jodi Marie, Kazoullis Andrea, Farah Camile Selim
Oral Biology and Pathology, School of Dentistry, The University of Queensland, St Lucia, 4072, Australia.
Front Biosci. 2008 May 1;13:5345-58. doi: 10.2741/3085.
Oral candidiasis is a significant health problem in terms of both morbidity and economic outlay. Infections are predominantly caused by the commensal C. albicans, and affect immunocompromised individuals, including HIV-positive and AIDS patients, organ transplant recipients and chemotherapy patients. The molecular and cellular immune mechanisms involved in protection from and responses to oral candidiasis are overlapping, but distinct from those associated with other manifestations of the disease, including systemic, vaginal and gastric candidiasis. In oral candidiasis, clinical observations and experimental mouse models suggest a critical role for cell-mediated immunity. In mice, CD4+ T-cells and the p40 subunit of interleukins 12 and 23 are strict prerequisites for resistance; however abrogation of IFN-gamma does not confer susceptibility. Here, we discuss this apparent inconsistency, and review the experimental evidence that clarifies which immune pathways are specifically involved in resistance and responses to candidiasis of the oral cavity. We also highlight deficiencies in the literature, particularly concerning the putative roles of some relatively new elements in immunobiology: interleukin-23, interleukin-17 and T helper (Th)17 cells.
就发病率和经济支出而言，口腔念珠菌病是一个重大的健康问题。感染主要由共生的白色念珠菌引起，影响免疫功能低下的个体，包括艾滋病毒阳性和艾滋病患者、器官移植受者和化疗患者。参与预防口腔念珠菌病以及对其作出反应的分子和细胞免疫机制相互重叠，但与该疾病的其他表现形式（包括系统性、阴道和胃部念珠菌病）相关的机制不同。在口腔念珠菌病中，临床观察和实验小鼠模型表明细胞介导的免疫起关键作用。在小鼠中，CD4 + T细胞以及白细胞介素12和23的p40亚基是抵抗的严格先决条件；然而，干扰素-γ的缺失并不会导致易感性。在此，我们讨论这种明显的不一致性，并回顾阐明哪些免疫途径具体参与口腔念珠菌病的抵抗和反应的实验证据。我们还强调了文献中的不足之处，特别是关于免疫生物学中一些相对较新的元素：白细胞介素-23、白细胞介素-17和辅助性T（Th）17细胞的假定作用。
