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微小隐孢子虫与小鼠树突状细胞相互作用导致其激活和寄生虫向肠系膜淋巴结的迁移。

Interaction of Cryptosporidium parvum with mouse dendritic cells leads to their activation and parasite transportation to mesenteric lymph nodes.

机构信息

Division of Infectious Diseases, Department of Biomedical Sciences, Tufts University Cummings School of Veterinary Medicine, North Grafton, MA, USA.

出版信息

Pathog Dis. 2014 Feb;70(1):17-27. doi: 10.1111/2049-632X.12078. Epub 2013 Sep 10.

DOI:10.1111/2049-632X.12078
PMID:23913680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4426866/
Abstract

Dendritic cells (DCs) are the antigen-presenting cells capable of activating naïve T cells. Although CD4+ T cells are crucial for Cryptosporidium parvum clearance, little is known about the role of DCs in the immune response to this parasite. In this study, the interaction between mouse DCs and C. parvum was investigated both in vitro and in vivo. For in vitro experiments, mouse bone marrow-derived dendritic cells (BMDCs) derived from wild-type C57B1/6 or MyD88-/- or C3H/HeJ mice and DC cell line DC2.4 were pulsed with C. parvum. Active invasion of parasites was demonstrated by parasite colocalization with host cell membranes and actin-plaque formation at the site of attachment. DC activation induced by the parasite invasion was demonstrated by upregulation of costimulatory molecules CD40, CD80, and CD86, as well as inflammatory cytokines IL-12, TNF-α, and IL-6. BMDCs derived from MyD88-/- and C3H/HeJ mice failed to produce IL-12 in response to C. parvum, suggesting the importance of TLR-dependent signaling pathway specially presence of a functional TLR4 pathway, for C. parvum-induced cytokine production. In vivo experiments showed that both parasite antigens and live parasites were transported to mice mesenteric lymph nodes. All together, these data suggest that DCs play a key role in host immune responses to C. parvum and pathogenesis of the disease.

摘要

树突状细胞 (DCs) 是能够激活初始 T 细胞的抗原呈递细胞。尽管 CD4+ T 细胞对于清除微小隐孢子虫至关重要,但对于 DCs 在针对这种寄生虫的免疫反应中的作用知之甚少。在这项研究中,研究了小鼠 DCs 与微小隐孢子虫之间的相互作用,包括在体外和体内。对于体外实验,从小鼠骨髓中衍生出的树突状细胞(BMDCs),来自野生型 C57B1/6 或 MyD88-/-或 C3H/HeJ 小鼠和 DC 细胞系 DC2.4,并与微小隐孢子虫孵育。通过寄生虫与宿主细胞膜的共定位以及附着部位肌动蛋白斑的形成,证明了寄生虫的主动入侵。寄生虫入侵诱导的 DC 激活表现为共刺激分子 CD40、CD80 和 CD86 的上调,以及炎性细胞因子 IL-12、TNF-α 和 IL-6 的产生。来自 MyD88-/-和 C3H/HeJ 小鼠的 BMDCs 无法响应微小隐孢子虫产生 IL-12,这表明 TLR 依赖性信号通路,特别是功能性 TLR4 通路的存在,对于微小隐孢子虫诱导的细胞因子产生非常重要。体内实验表明,寄生虫抗原和活寄生虫都被运送到小鼠肠系膜淋巴结。所有这些数据表明,DCs 在宿主对微小隐孢子虫的免疫反应和疾病发病机制中发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0aa/4426866/83c0d5f705bf/nihms515605f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0aa/4426866/83c0d5f705bf/nihms515605f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0aa/4426866/c7b069244e83/nihms515605f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0aa/4426866/628d194c4925/nihms515605f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0aa/4426866/b990d31087c4/nihms515605f3.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0aa/4426866/83c0d5f705bf/nihms515605f7.jpg

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