摘要
This study analyzes the phenotype of vaginal dendritic cells (VDCs), their antigenic presentation and activation of T-cell cytokine secretion, and their protective role in a rat model of Candida vaginitis. Histological observation demonstrated a significant accumulation of OX62(+) VDCs in the mucosal epithelium of Candida albicans-infected rats at the third round of infection. We identified two subsets of OX62(+) VDCs differing in the expression of CD4 molecule in both noninfected and Candida-infected rats. The OX62(+) CD4(+) subset of VDCs displayed a lymphoid cell-like morphology and expressed the T-cell antigen CD5, whereas the OX62(+) CD4(-) VDC subset exhibited a myeloid morphology and was CD5 negative. Candida infection resulted in VDC maturation with enhanced expression of CD80 and CD134L on both CD4(+) and CD4(-) VDC subsets at 2 and 6 weeks after Candida infection. CD5(-) CD4(-) CD86(-) CD80(-) CD134L(+) VDCs from infected, but not noninfected, rats spontaneously released large amounts of interleukin-12 (IL-12) and tumor necrosis factor alpha, whereas all VDC subsets released comparable levels of IL-10 and IL-2 cytokines. Furthermore, OX62(+) VDCs from infected rats primed naive CD4(+) T-cell proliferation and release of cytokines, including gamma interferon, IL-2, IL-6, and IL-10, in response to staphylococcal enterotoxin B stimulation in vitro. Adoptive transfer of highly purified OX62(+) VDCs from infected rats induced a significant acceleration of fungal clearance compared with that in rats receiving naive VDCs, suggesting a protective role of VDCs in the anti-Candida mucosal immunity. Finally, VDC-mediated protection was associated with their ability to rapidly migrate to the vaginal mucosa and lymph nodes, as assessed by adoptive transfer of OX62(+) VDCs labeled with 5 (and 6-)-carboxyfluorescein diacetate succinimidyl ester.
摘要译文
这项研究中分析了阴道树突细胞（VDC可以），T细胞的细胞因子分泌的抗原表现和活化的表型，和在念珠菌的大鼠模型的保护作用阴道炎。组织学观察证实OX62的白色念珠菌感染的大鼠粘膜上皮显著的积累（）VDC能够在第三轮感染。我们确定了OX62的两个子集（）VDC可以在不同的CD4分子的两个未感染和念珠菌感染的大鼠的表达。VDC能够的OX62（）的CD4（）的子集显示在淋巴细胞样的形态和表达的T细胞抗原CD5，而OX62（）CD4（ - ）VDC集展出了粒细胞的形态，是CD5阴性。念珠菌感染导致VDC成熟与CD80和CD134L对两者的CD4（）和CD4的表达增强（ - ）直流电压，在2和6周念珠菌感染后的子集。CD5（ - ）CD4（ - ）CD86（ - ）CD80（ - ）CD134L（）VDC可以从感染的，但不是非感染，大鼠自发释放大量白介素-12（IL-12），肿瘤坏死因子α的，而释放的IL-10和IL-2细胞因子的水平相当的所有直流的子集。此外，OX62（）从引物的细胞因子的幼稚的CD4（）的T细胞增殖和释放感染大鼠VDC能够，包括γ干扰素，IL-2，IL-6，和IL-10中，响应于葡萄球菌肠毒素B的刺激体外。高纯度的OX62的过继转移（）从被感染的老鼠VDC的诱导显著加速真菌间隙与大鼠接受幼稚VDC的比较，暗示VDC能够在抗念珠菌粘膜免疫保护作用。最后，VDC介导的保护用他们的迅速迁移到阴道粘膜和淋巴结的能力有关，作为评估OX62的过继转移（）VDC的标记5（和6 - ） - 羧基二醋酸琥珀酰亚胺酯。
De Bernardis F; Lucciarini R; Boccanera M; Amantini C; Arancia S; Morrone S; Mosca M; Cassone A; Santoni G. Phenotypic and functional characterization of vaginal dendritic cells in a rat model of Candida albicans vaginitis.[J]. Infection and Immunity, 2006,74(7): 4282-4294