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Daniel J Atwood¹, Zhibin He¹, Makoto Miyazaki²

¹Renal Division, Rocky Mountain Regional Veteran's Affairs (VA) Medical Center, Aurora, CO, United States.

Frontiers in immunology

|June 11, 2025

概括

三级淋巴组织 (TLT) 在非淋巴组织中形成. 在缺乏与自相关的7 (Atg7) 的老年小鼠中,脏产生了大型TLT. 由p-S6标记的mTORC1活性驱动免疫细胞的增殖和TLT在这些组织中的生长.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
腎病理生理學腎病理生理學

背景情况:

三级淋巴组织 (TLT) 是异位淋巴组织结构,在炎症或损伤期间在非淋巴组织中出现.
与自相关的7 (Atg7) 在细胞平衡中起作用,其缺乏可以导致病理.
拉巴胺素复合体1 (mTORC1) 途径的机械性标是细胞生长,增殖和免疫反应的关键调节者.

研究的目的:

研究与自相关的7 (Atg7) 缺陷和mTORC1信号在中三级淋巴细胞组织 (TLT) 的形成和发育中的作用.
为了确定mTORC1在管或TLT中的活性是否驱动TLT的形成.
探索mTOR抑制剂在病模型中调节TLT发育的治疗潜力.

主要方法:

产生管特定的Atg7淘汰赛小鼠来研究TLT形成.
从老年Atg7淘汰赛小鼠,多囊性病 (Pkd1^RC/RC) 小鼠和缺血性脏分析TLT存在和p-S6表达.
用Torin2,一种mTOR抑制剂治疗Pkd1^RC/RC和缺血性模型,并评估TLT的大小和数量.
利用管体特定的Atg7^-/-猛禽 (mTORC1)^-/-小鼠来区分管体与TLT mTORC1信号的作用.

主要成果:

患有管特异性Atg7淘汰症的老年小鼠在脏中表现出大量的大型TLT.
在各种损伤模型中,在管和TLT中观察到升高的p-S6,mTORC1激活的标志物.
用Torin2治疗显著减少了Pkd1^RC/RC和缺血性脏中的TLT形成,与p-S6抑制相关.
管管特定的mTORC1 (猛禽) 淘汰对TLT发育的影响很小,这表明TLT中的mTORC1活性至关重要.

结论:

特别是在三级淋巴细胞组织 (TLT) 内的p-S6活性,而不是管,驱动免疫细胞的增殖并促进TLT的形成和生长.
在损伤和衰老的背景下,mTORC1信号传递是TLT发展的关键驱动力.
mTOR抑制剂代表了一种有前途的治疗策略,用于管理与异常TLT形成相关的疾病.

关键词:

自自是自的过程.在mTOROR中使用mTOR.在P62上,P62就是P62 多囊性脏多囊性脏三级淋巴状组织的第三级淋巴状组织.

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