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CD207+ Langerhans cells constitute a minor population of skin-derived antigen-presenting cells in the draining lymph node following exposure to Schistosoma mansoni

机译:暴露于曼氏血吸虫后CD207 +朗格汉斯细胞在引流淋巴结中构成了一小部分皮肤来源的抗原呈递细胞

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摘要

Infectious cercariae of Schistosoma mansoni gain entry to the mammalian host through the skin where they induce a transient inflammatory influx of mononuclear cells. Some of these cells have antigen-presenting cell function (MHCII+) and have been reported to migrate to the skin-draining lymph nodes (sdLN) where they have the potential to prime CD4+ cells of the acquired immune response. Here, in mice exposed to vaccinating radiation-attenuated schistosome larvae, which induce high levels of protective immunity to challenge infection, we describe the parasite-induced migration of Langerhans cells (LCs) from the epidermal site of immunisation to the sdLN using a specific monoclonal antibody that recognises langerin (CD207). CD207+ cells with dendritic morphology were abundant in the epidermis at all times and their migration into the dermis was detected soon after vaccination. All CD207+ LCs were MHCII+ but not all MHCII+ cells in the skin were CD207+. LCs migrated from the dermis in enhanced numbers after vaccination, as detected in dermal exudate populations recovered after in vitro culture of skin biopsies. Elevated numbers of CD207+ LCs were also detected in the sdLN from 24 h to 4 days after vaccination. However, compared with other dermal-derived antigen-presenting cells that were CD207MHCII+ or CD207CD11c+, the relative numbers of CD207+ cells in the dermal exudate population and in the sdLN were very small. Furthermore, the migration of CD207+ cells after exposure to ‘protective’ radiation-attenuated, compared with ‘non-protective’ normal cercariae, was similar in terms of numbers and kinetics. Together, these studies suggest that CD207+ LCs are only a minor component of the antigen-presenting cell population that migrates from the epidermis and they are unlikely to be important in the priming of protective CD4+ cells in the sdLN.
机译:曼氏血吸虫的传染性尾c通过皮肤进入哺乳动物宿主,在那里它们诱导单核细胞的瞬时炎性流入。这些细胞中的一些具有抗原呈递细胞功能(MHCII + ),据报道会迁移到皮肤引流淋巴结(sdLN),在那里它们可能引发CD4 + < / sup>获得性免疫反应的细胞。在这里,在暴露于疫苗的辐射衰减的血吸虫幼虫中诱导高水平的保护性免疫以挑战感染的小鼠中,我们描述了寄生虫诱导的朗格汉斯细胞(LC)从免疫的表皮部位向sdLN的迁移,使用了特定的单克隆抗体识别橘皮素的抗体(CD207)。具有树突状形态的CD207 + 细胞在任何时候都在表皮中丰富,并且在接种疫苗后不久就检测到它们向真皮的迁移。皮肤中所有的CD207 + LC均为MHCII + ,但并非所有皮肤中的MHCII + 细胞均为CD207 + 。接种疫苗后,LCs从真皮中迁移的数量增加,这是在皮肤活检组织的体外培养后回收的真皮渗出液中检测到的。接种疫苗后24小时至4天,sdLN中还检测到CD207 + LC数量升高。但是,与其他真皮来源的抗原呈递细胞相比,CD207 - MHCII + 或CD207 - CD11c + ,真皮分泌物群体和sdLN中CD207 + 细胞的相对数量非常少。此外,与“非保护性”正常尾c相比,暴露于“保护性”辐射衰减后的CD207 + 细胞的迁移在数量和动力学上相似。总之,这些研究表明,CD207 + LC仅是从表皮迁移的抗原呈递细胞群体的一小部分,它们不太可能在保护性CD4 +的启动中起重要作用。 sdLN中的单元格。

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