Cell Metab:为什么越老越怕冷?免疫细胞来“背锅”。

2021-09-05 haibei MedSci原创

IL-33会促进致病的ILC2s增殖,这些ILC2s有内在的缺陷,会促进促炎症反应和降低脂肪组织的恢复能力,而移植成年ILC2s则足以保护老年小鼠免受寒冷。

越来越多的证据表明,免疫系统是通过控制炎症的免疫代谢检查点来维持脂肪组织稳态的关键节点。脂肪驻留的免疫细胞负责控制内脏脂肪组织(VAT)的炎症,并调节禁食诱导的脂肪分解、冷诱导的产热和胰岛素抵抗。虽然几十年的研究已经指出了抗微生物免疫反应的先天和适应性免疫方面的许多缺陷,但只有有限的研究探索了负责维持组织平衡的组织驻留免疫细胞如何调节衰老过程和对压力的恢复能力。

脂肪组织老化的特点是炎症加剧、轻度胰岛素抵抗和禁食诱导的脂肪分解抵抗。虽然这些表型在肥胖人群的脂肪组织中也是共有的,但有一些重要的差异区分了衰老与肥胖的脂肪。这些差异中包括不同免疫群体的组成和活动:调节性T细胞(Tregs)在肥胖个体中具有保护作用,但它们的积累在衰老过程中是有害的;脂肪B细胞会获得独特的衰老表型,与机体不耐寒有关;促炎性巨噬细胞在肥胖脂肪组织中占主导,而老年脂肪组织表现出M2样巨噬细胞的损失和脂肪分解的抑制。

衰老会损害机体的综合免疫代谢反应,这些反应已经进化到维持机体的核心体温,以便帮助机体在寒冷压力、感染和饮食限制下生存。脂肪组织炎症调节生热应激反应,但目前,脂肪组织驻留细胞如何在老年群体中帮助产热还不清楚。此外,在衰老的脂肪组织中,单细胞分辨率的组织驻留免疫细胞转录组的详细描述还没有被定义。

衰老脂肪组织中免疫细胞异常,产热减少

最近,研究人员报告了脂肪组织驻留白细胞群的年龄相关变化,包括2组先天性淋巴细胞(ILC2s)的急剧损失。通过补充IL-33可以使老年小鼠的ILC2数量恢复到成年时的水平,但未能挽救老年小鼠的代谢障碍和寒冷引起的死亡增加。

转录组分析显示了老年ILC2的内在缺陷:研究人员发现在衰老过程中,IL-33会促进致病的ILC2s增殖,这些ILC2s有内在的缺陷,会促进促炎症反应和降低脂肪组织的恢复能力,而移植成年ILC2s则足以保护老年小鼠免受寒冷

因此,在衰老过程中,脂肪组织的ILC2s的功能缺陷驱动了产热失败

 

原始出处:

Emily L. Goldberg et al. IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2. Cell Metabolism (2021). 

 

 

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    2022-07-23 guojianrong
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    2021-11-13 维他命
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    2022-03-06 一闲
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    2021-09-06 ms6000001624652641

    免疫很重要

    0

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    2021-09-05 滕双娇

    学习

    0

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