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绦虫抗原诱导人树突状细胞产生耐受性样表型,并抑制 LPS 炎症反应。

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

机构信息

Biomedicine Unit, Facultad de Estudios Superiores Iztacala, UNAM, México City, México.

出版信息

Int J Biol Sci. 2011;7(9):1391-400. doi: 10.7150/ijbs.7.1391. Epub 2011 Nov 1.

Abstract

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.

摘要

寄生虫为了在体内更好地生存,会进化出一些策略来改变树突状细胞(DCs)的表型,并损害其功能。不同研究中,人们对 DCs 针对蠕虫及其衍生物的反应存在差异。在这里,我们发现猪带绦虫(Taenia crassiceps)的排泄/分泌产物(TcES)并不会诱导人源 DCs 的成熟,因为其表面 CD83、HLA-DR、CD80 和 CD86 分子的表达并未增加,反而增强了 IL-10 的产生,并正向调节 C 型凝集素受体 MGL 的表达,负向调节 DC-SIGN 的表达。此外,这些抗原能够下调 LPS 诱导的这些细胞的炎症反应,降低成熟标志物的表达和促炎细胞因子 IL-1β、TNF、IL-12 和 IL-6 的产生。如果在 DCs 分化过程中暴露于这些寄生虫抗原,TcES 对 LPS 反应的影响更强。总的来说,这些发现表明 TcES 具有诱导人源 DCs 分化为耐受性表型并抑制炎症刺激物作用的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe39/3221946/f5f894a59cde/ijbsv07p1391g01.jpg

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