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Cestode antigens induce a tolerogenic-like phenotype and inhibit LPS in-flammatory responses in human dendritic cells

机译:Cestode抗原诱导人类树突状细胞产生致耐受性表型并抑制LPS炎症反应

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Pathogens have developed strategies to modify Dendritic Cells (DCs) phenotypes and impair their functions in order to create a safer environment for their survival. DCs responses to helminths and their derivatives vary among different studies. Here we show that excretory/secretory products of the cestode Taenia crassiceps (TcES) do not induce the maturation of human DCs judged by a lack of increment in the expression of CD83, HLA-DR, CD80 and CD86 molecules but enhanced the production of IL-10 and positively modulated the expression of the C-type lectin receptor MGL and negatively modulated the expression of DC-SIGN. Additionally, these antigens were capable of down-modulating the inflammatory response induced by LPS in these cells by reducing the expression of the maturation markers and the production of the inflammatory cytokines IL-1β, TNF, IL-12 and IL-6. The effects of TcES upon the DCs responses to LPS were stronger if cells were exposed during their differentiation to the helminth antigens. All together, these findings suggest the ability of TcES to induce the differentiation of human DCs into a tolerogenic-like phenotype and to inhibit the effects of inflammatory stimuli.
机译:病原体已开发出策略来修饰树突状细胞(DC)表型并损害其功能,从而为其生存创造更安全的环境。 DC对蠕虫及其衍生物的反应在不同的研究中有所不同。在这里,我们表明,由CD83,HLA-DR,CD80和CD86分子表达不足的增加判断,猪est虫en虫(Tenia crassiceps,TcES)的排泄/分泌产物不会诱导人DC的成熟,但可以增强IL的产生-10和正调节C型凝集素受体MGL的表达而负调节DC-SIGN的表达。另外,这些抗原能够通过减少成熟标志物的表达和炎性细胞因子IL-1β,TNF,IL-12和IL-6的产生来下调LPS在这些细胞中诱导的炎性反应。如果细胞在分化过程中接触蠕虫抗原,则TcES对DC对LPS响应的影响会更强。总之,这些发现表明TcES具有诱导人DC分化为致耐受性表型并抑制炎性刺激作用的能力。

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