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在TNF-TNFR-TRAF6轴中介于的NF-κB依赖于DIV1的抗病毒免疫力

Xuzheng Liao¹, Sihong Liu², Shihan Chen²

¹State Key Laboratory of Biocontrol/Southern Marine Science and Engineering Guangdong Laboratory (Zhuhai), School of Marine Sciences, Sun Yat-sen University, Guangzhou, PR China; Guangdong Provincial Key Laboratory for Aquatic Economic Animals, School of Life Sciences, Sun Yat-sen University, Guangzhou, PR China.

International journal of biological macromolecules

|November 27, 2025

概括

瘤亡因子受体 (LvTNFR) 和其连接体LvTNF对于抗十足色病毒1 (DIV1) 的抗病毒防御至关重要. 这个信号轴激活NF-κB,增强的免疫力.

科学领域:

免疫学免疫学免疫学
无脊椎动物生物学无脊椎动物生物学
分子生物学分子生物学

背景情况:

瘤亡因子 (TNF) 和它的受体 (TNFR) 信号传递对于脊椎动物免疫是至关重要的.
目前尚不清楚TNF-TNFR在无脊椎动物抗病毒防御中的作用.

研究的目的:

在 (Litopenaeus vannamei) 中识别和表征瘤亡因子受体 (LvTNFR).
调查LvTNF-LvTNFR轴在抗病毒防御中对十足虹色病毒1 (DIV1) 的作用.

主要方法:

对LvTNFR的遗传学分析.
基因表达分析 (感染后升高调节).
RNA干扰 (RNAi) 来评估基因功能.
蛋白质与蛋白质相互作用试验 (LvTNFR-LvTRAF6).
功能性测试 (NF-κB激活,抗微生物诱导).
转录组简介. 转录组简介.

主要成果:

在中发现的LvTNFR,缺乏DEATH域,但具有TRAF结合动机.
在DIV1感染后,LvTNF和LvTNFR的表达增加.
沉默LvTNF或LvTNFR导致病毒复制增加和的存活率降低.
LvTNFR与LvTRAF6相互作用,形成一个TNF-TNFR-TRAF6信号轴.
这个轴激活LvDorsal (NF-κB同源),促进核转位和抗菌的表达.
PHLPP被确定为影响NF-κB激活的下游效应因子.

结论:

在中存在一个保存的TNF-TNFR-TRAF6信号轴,这对抗病毒免疫至关重要.
这一途径激活NF-κB,诱导抗微生物的产生.
这些发现提供了对无脊椎动物抗病毒免疫力的机制性见解.
这个轴代表了开发抗病品种的潜在遗传标.

关键词:

抗病毒免疫抗病毒免疫 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV1 DIV2 DIV2 DIV2 DIV2 DIV2 DIV2 DIV3 DIV4 DIV5 DIV6 DIV7 利托佩内亚斯 (Litopenaeus vannamei) 是一个水族群.这就是NF-κBB.在TNFTNFR轴上.在TRAF6中,转录组转录组就是一个转录组.

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