| Literature DB >> 31735593 |
Christina D Camell1, Patrick Günther2, Aileen Lee1, Emily L Goldberg1, Olga Spadaro1, Yun-Hee Youm1, Andrzej Bartke3, Gene B Hubbard4, Yuji Ikeno5, Nancy H Ruddle6, Joachim Schultze2, Vishwa Deep Dixit7.
Abstract
During aging, visceral adiposity is often associated with alterations in adipose tissue (AT) leukocytes, inflammation, and metabolic dysfunction. However, the contribution of AT B cells in immunometabolism during aging is unexplored. Here, we show that aging is associated with an expansion of a unique population of resident non-senescent aged adipose B cells (AABs) found in fat-associated lymphoid clusters (FALCs). AABs are transcriptionally distinct from splenic age-associated B cells (ABCs) and show greater expansion in female mice. Functionally, whole-body B cell depletion restores proper lipolysis and core body temperature maintenance during cold stress. Mechanistically, the age-induced FALC formation, AAB, and splenic ABC expansion is dependent on the Nlrp3 inflammasome. Furthermore, AABs express IL-1R, and inhibition of IL-1 signaling reduces their proliferation and increases lipolysis in aging. These data reveal that inhibiting Nlrp3-dependent B cell accumulation can be targeted to reverse metabolic impairment in aging AT.Entities:
Keywords: B cell depletion; IL-1 signaling; Nlrp3 inflammasome; adipose tissue B cells; age-associated B cells; aging; fat-associated lymphoid cluster; growth hormone receptor; inflammaging; lipolysis
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Year: 2019 PMID： 31735593 PMCID： PMC6944439 DOI： 10.1016/j.cmet.2019.10.006
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287