Ponte-Sucre A, Heise D, Moll H
Laboratory of Molecular Physiology, Instituto de Medicina Experimental, Cátedra de Fisiología, Facultad de Medicina, Universidad Central de Venezuela, Venezuela.
Immunology. 2001 Dec;104(4):462-7. doi: 10.1046/j.1365-2567.2001.01333.x.
Langerhans cells (LC), members of the dendritic cell family, play a central role in the initiation and regulation of the immune response against the protozoan parasite Leishmania major. LC take up antigens in the skin and transport them to the regional lymph nodes for presentation to T cells. However, it is not known whether LC functions are modulated by parasite antigens. In the present study, we examined the effect of a major parasite surface molecule, L. major lipophosphoglycan (LPG), on the maturation of LC and their migratory properties. The results show that exposure to LPG did not affect the expression of major histocompatibility complex (MHC) class II and B7, but induced an up-regulation of CD25, CD31 and vascular endothelial (VE)-cadherin expression and a down-regulation of Mac-1 expression, by LC. Importantly, LPG treatment inhibited the migratory activity of LC, as it reduced their efflux from skin explants and their migration in transwell cultures. These results suggest that Leishmania LPG impairs LC migration out of the skin and thus may modulate their immunostimulatory functions, which require LC translocation from skin to lymph nodes.
朗格汉斯细胞(LC)是树突状细胞家族的成员,在针对原生动物寄生虫硕大利什曼原虫的免疫反应的启动和调节中发挥核心作用。LC在皮肤中摄取抗原,并将其转运至局部淋巴结以呈递给T细胞。然而,尚不清楚LC的功能是否受到寄生虫抗原的调节。在本研究中,我们检测了一种主要的寄生虫表面分子——硕大利什曼原虫脂磷壁酸聚糖(LPG)对LC成熟及其迁移特性的影响。结果显示,暴露于LPG并不影响主要组织相容性复合体(MHC)II类分子和B7的表达,但可诱导LC上调CD25、CD31和血管内皮(VE)-钙黏蛋白的表达,并下调Mac-1的表达。重要的是,LPG处理抑制了LC的迁移活性,因为它减少了LC从皮肤外植体的流出及其在Transwell培养中的迁移。这些结果表明,利什曼原虫LPG损害了LC从皮肤的迁出,因此可能调节其免疫刺激功能,而这需要LC从皮肤转运至淋巴结。