美国耶鲁大学Vishwa Deep Dixit研究组发现衰老诱导脂肪B细胞Nlrp3炎性小体依赖性扩张，并破坏代谢稳态。 该研究于2019年11月14日在线发表在《细胞—代谢》上。

研究人员发现衰老与在脂肪相关淋巴样簇（FALCs）中发现的特异驻留非衰老老年脂肪B细胞（AAB）的扩张有关。AAB在转录上不同于脾脏年龄相关性B细胞（ABC），并在雌性小鼠中显示出更大的扩增。从功能上讲，全身B细胞耗竭可在冷应激期间恢复适当的脂解作用和维持核心体温。从机理上讲，年龄引起的FALC形成、AAB和脾脏ABC扩张取决于Nlrp3炎性体。此外，AAB表达IL-1R并且抑制IL-1信号传导，这会减少其增殖并增加衰老过程中的脂解作用。这些数据表明抑制Nlrp3依赖的B细胞积累可以靶向逆转衰老AT的代谢损伤。

此外，在衰老过程中，内脏脂肪通常与脂肪组织（AT）白细胞改变、炎症和代谢功能障碍有关。然而，衰老过程中AT B细胞在免疫代谢中的作用仍未阐明。

附：英文原文

Title: Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis

Author: Christina D. Camell, Patrick Günther, Aileen Lee, Emily L. Goldberg, Olga Spadaro, Yun-Hee Youm, Andrzej Bartke, Gene B. Hubbard, Yuji Ikeno, Nancy H. Ruddle, Joachim Schultze, Vishwa Deep Dixit

Issue&Volume: November 14, 2019

Abstract: During aging, visceral adiposity is often associated with alterations in adipose tissue(AT) leukocytes, inflammation, and metabolic dysfunction. However, the contributionof AT B cells in immunometabolism during aging is unexplored. Here, we show that agingis associated with an expansion of a unique population of resident non-senescent agedadipose B cells (AABs) found in fat-associated lymphoid clusters (FALCs). AABs aretranscriptionally distinct from splenic age-associated B cells (ABCs) and show greaterexpansion in female mice. Functionally, whole-body B cell depletion restores properlipolysis and core body temperature maintenance during cold stress. Mechanistically,the age-induced FALC formation, AAB, and splenic ABC expansion is dependent on theNlrp3 inflammasome. Furthermore, AABs express IL-1R, and inhibition of IL-1 signalingreduces their proliferation and increases lipolysis in aging. These data reveal thatinhibiting Nlrp3-dependent B cell accumulation can be targeted to reverse metabolicimpairment in aging AT.

DOI: 10.1016/j.cmet.2019.10.006

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30561-3