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双链 RNA 通过 TRIF 和 NF-κB 诱导鸡 T 细胞淋巴瘤细胞凋亡。

Double-stranded RNA induces chicken T-cell lymphoma apoptosis by TRIF and NF-κB.

机构信息

Ministry of Education Key Lab for Avian Preventive Medicine, Yangzhou University, No. 12 East Wenhui Road, Yangzhou, Jiangsu, 225009, P. R. China.

Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, No. 12 East Wenhui Road, Yangzhou, Jiangsu, 225009, P. R. China.

出版信息

Sci Rep. 2017 Aug 8;7(1):7547. doi: 10.1038/s41598-017-07919-w.

DOI:10.1038/s41598-017-07919-w
PMID:28790362
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5548913/
Abstract

Toll-like receptor-3 (TLR3), a member of the pathogen recognition receptor family, has been reported to activate immune response and to exhibit pro-apoptotic activity against some tumor cells. However it is unclear whether TLR3 has same function against chicken lymphoma. In this paper we investigated the effect of TLR3 activation on a Marek's disease lymphoma-derived chicken cell line, MDCC-MSB1. The TLR3 agonist poly (I:C) activated TLR3 pathway and inhibited tumor cells proliferation through caspase-dependent apoptosis. Using pharmacological approaches, we found that an interferon-independent mechanism involving Toll-IL-1-receptor domain-containing adapter-inducing IFN-α (TRIF) and nuclear factor κB (NF-κB) causes the apoptosis of MDCC-MSB1 cells. This is the first report about the function of TLR3 in chicken T-cell lymphoma, especially in signal pathway. The mechanisms underlying TLR3-mediated apoptosis may contribute to the development of new drug to treat lymphomas and oncovirus infections.

摘要

Toll 样受体 3（TLR3）是病原体识别受体家族的成员之一，据报道，它可以激活免疫反应，并对一些肿瘤细胞表现出促凋亡活性。然而，TLR3 是否对鸡淋巴瘤具有相同的功能尚不清楚。在本文中，我们研究了 TLR3 激活对马立克氏病淋巴瘤衍生的鸡细胞系 MDCC-MSB1 的影响。TLR3 激动剂聚（I：C）通过 caspase 依赖性细胞凋亡激活 TLR3 途径并抑制肿瘤细胞增殖。通过药理学方法，我们发现一种干扰素非依赖性机制涉及 Toll-IL-1-受体域包含衔接诱导 IFN-α（TRIF）和核因子 κB（NF-κB）导致 MDCC-MSB1 细胞凋亡。这是 TLR3 在鸡 T 细胞淋巴瘤中，特别是在信号通路中的功能的首次报道。TLR3 介导的细胞凋亡的机制可能有助于开发治疗淋巴瘤和致癌病毒感染的新药。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/430f7a2d7abb/41598_2017_7919_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/05e84156578f/41598_2017_7919_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/e3a4fe6ee921/41598_2017_7919_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/a31a3574dc2a/41598_2017_7919_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/6a646943579c/41598_2017_7919_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/430f7a2d7abb/41598_2017_7919_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/05e84156578f/41598_2017_7919_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/e3a4fe6ee921/41598_2017_7919_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/a31a3574dc2a/41598_2017_7919_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/6a646943579c/41598_2017_7919_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7443/5548913/430f7a2d7abb/41598_2017_7919_Fig5_HTML.jpg

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