美国耶鲁大学Vishwa Deep Dixit和加州大学旧金山分校Emily L. Goldberg研究组合作取得最新进展。他们表明IL-33 通过扩大功能失调的脂肪2 型先天淋巴细胞 (ILC2) 导致衰老过程中产热衰竭。这一研究成果于2021年9月1日发表在国际顶尖学术期刊《细胞—代谢》上。
他们定义了脂肪驻留免疫系统的变化，并确定了ILC2在衰老过程中丢失。通过补充 IL-33 将老年小鼠的 ILC2 数量恢复到成年小鼠水平，但未能挽救老年小鼠的代谢障碍和增加寒冷诱导的致死率。转录组学分析揭示了老年 ILC2 的内在缺陷，成年 ILC2 的过继转移足以保护老年小鼠免受寒冷。因此，衰老过程中脂肪 ILC2 的功能缺陷会导致产热衰竭。
据介绍，衰老会损害综合免疫代谢反应，这些反应已经进化为维持恒温动物核心体温，使其在寒冷应激、感染和饮食限制中存活下来。脂肪组织炎症调节产热应激反应，但脂肪组织驻留细胞如何引发老年人的产热衰竭尚不清楚。
附：英文原文
Title: IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2
Author: Emily L. Goldberg, Irina Shchukina, Yun-Hee Youm, Seungjin Ryu, Takeshi Tsusaka, Kyrlia C. Young, Christina D. Camell, Tamara Dlugos, Maxim N. Artyomov, Vishwa Deep Dixit
Issue&Volume: 2021-09-01
Abstract: Aging impairs the integrated immunometabolic responses, which have evolved to maintaincore body temperature in homeotherms to survive cold stress, infections, and dietaryrestriction. Adipose tissue inflammation regulates the thermogenic stress response,but how adipose tissue-resident cells instigate thermogenic failure in the aged areunknown. Here, we define alterations in the adipose-resident immune system and identifythat type 2 innate lymphoid cells (ILC2s) are lost in aging. Restoration of ILC2 numbersin aged mice to levels seen in adults through IL-33 supplementation failed to rescueold mice from metabolic impairment and increased cold-induced lethality. Transcriptomicanalyses revealed intrinsic defects in aged ILC2, and adoptive transfer of adult ILC2sare sufficient to protect old mice against cold. Thus, the functional defects in adiposeILC2s during aging drive thermogenic failure.
DOI: 10.1016/j.cmet.2021.08.004
Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(21)00367-3
Cell Metabolism：《细胞—代谢》，创刊于2005年。隶属于细胞出版社，最新IF：31.373
官方网址：https://www.cell.com/cell-metabolism/home
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本期文章：《细胞—代谢》：Online/在线发表
