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细粒棘球绦虫包虫囊液对树突状细胞分化和细胞因子分泌的调节作用

Modulation of dendritic cell differentiation and cytokine secretion by the hydatid cyst fluid of Echinococcus granulosus.

作者信息

Kanan João H C, Chain Benjamin M

机构信息

Departamento de Microbiologia, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

出版信息

Immunology. 2006 Jun;118(2):271-8. doi: 10.1111/j.1365-2567.2006.02375.x.

DOI:10.1111/j.1365-2567.2006.02375.x
PMID:16771863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1782286/
Abstract

Chronic infection by Echinococcus granulosus results in establishment of fluid-filled cysts (hydatid cysts) in liver or lungs of infected hosts, which can escape destruction by the host immune system for long periods. This study explores the modulation by hydatid cyst fluid of the in vitro human monocyte to dendritic cell (DC) transition induced by granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). Addition of the fluid to adherent peripheral blood monocytes cultured in GM-CSF/IL-4 stimulates release of prostaglandin E2 (PGE2) and IL-6. Exposure of differentiating DC to the fluid during the 7-day culture in GM-CSF/IL-4 impairs their subsequent ability to secrete IL-12, IL-6 or PGE2 in response to lipopolysaccharide (LPS) stimulation. This inhibition is not dependent on the initial release of PGE2. The presence of hydatid cyst fluid also modulates the phenotype of the cells generated during culture, resulting in increased CD14 expression and decreased expression of CD1a. Finally, hydatid fluid can stimulate predifferentiated DC to mature, as evidenced by release of IL-12 and IL-6, and by up-regulation of class II major histocompatibility complex and CD86. The possible role of dendritic cell modulation in regulating the host immune response to hydatid cysts is discussed.

摘要

细粒棘球绦虫的慢性感染会导致受感染宿主的肝脏或肺部形成充满液体的囊肿(包虫囊肿),这些囊肿能够长期逃避宿主免疫系统的破坏。本研究探讨了包虫囊肿液对粒细胞巨噬细胞集落刺激因子(GM-CSF)和白细胞介素-4(IL-4)诱导的体外人单核细胞向树突状细胞(DC)转变的调节作用。将该液体添加到在GM-CSF/IL-4中培养的贴壁外周血单核细胞中,会刺激前列腺素E2(PGE2)和IL-6的释放。在GM-CSF/IL-4中进行7天培养期间,将分化中的DC暴露于该液体中,会损害它们随后响应脂多糖(LPS)刺激分泌IL-12、IL-6或PGE2的能力。这种抑制不依赖于PGE2的初始释放。包虫囊肿液的存在还会调节培养过程中产生的细胞的表型,导致CD14表达增加,CD1a表达减少。最后,包虫液可刺激预分化的DC成熟,这可通过IL-12和IL-6的释放以及II类主要组织相容性复合体和CD86的上调来证明。本文讨论了树突状细胞调节在调控宿主对包虫囊肿免疫反应中的可能作用。

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