超的压力诱导炎症和过度的Th17反应,对蒂拉皮亚的T细胞免疫力产生突发反应
Jiansong Zhang1, Xiaodan Wang1, Kang Li1
1State Key Laboratory of Estuarine and Coastal Research, School of Life Sciences, East China Normal University, Shanghai, China.
Journal of immunology (Baltimore, Md. : 1950)
|May 3, 2024
概括
超的压力引发炎症和过度的T细胞激活尼罗河鱼,增强Th17免疫反应和通过ROS和p38-MK2信号损害抗菌免疫力.
科学领域:
- * 免疫学 免疫学
- * 透生理学 透生理学
- * 环境压力反应反应
背景情况:
- * 骨鱼对T细胞免疫力对透应激的适应机制尚不清楚.
- *尼罗河鱼 (Oreochromis niloticus) 是一种能够承受广泛度范围的鱼.
研究的目的:
- * 为了研究T细胞对尼罗河鱼中超性应激的反应.
- *阐明T细胞激活和在高血压条件下的免疫反应中涉及的分子途径.
主要方法:
- * 尼罗河鱼暴露于高位压力.
- *分析T细胞激活标记物,细胞因子表达 (IL-17A,IL-6,TGF-β1) 和信号通路 (RORα,STAT3,p38-MK2,MKK6).
- * 评估细胞内活性氧物种 (ROS) 含量以及ROS消除和途径阻断对IL-17A产生的影响.
主要成果:
- *高血压导致炎症和过度的T细胞激活在小毛病.
- *增加IL-17A,RORα的表达和STAT3信号的激活,表明增强的Th17反应.
- *高压性压力增加了ROS,激活了p38-MK2通路,促进了IL-17A的产生和抗菌免疫力受损. 确定了一个积极的反循环,涉及促炎细胞因子和MKK6-p38-MK2轴.
结论:
- *这项研究揭示了T细胞免疫反应对早期脊椎动物高压的首次描述的机制.
- *这些发现突出了ROS和p38-MK2通路在调解T细胞对透应激反应中的作用.
- * 提供了关于T细胞在环境挑战下适应性演变的见解,以及对鱼类健康和水产养殖的潜在影响.
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