Matches in SemOpenAlex for { <https://semopenalex.org/work/W2936918230> ?p ?o ?g. }
- W2936918230 abstract "Summary Visceral adiposity in elderly is associated with alterations in adipose tissue immune cells leading to inflammation and metabolic dysfunction. The Nlrp3 inflammasome is a critical regulator of macrophage activation, inflammation, and immunometabolism in visceral adipose tissue during aging; however, the potential contribution of adipose tissue B cells is unexplored. Here, we show that aging expands adipose-resident B cells and fat-associated lymphoid clusters (FALCs) in visceral white adipose tissue. Adipose tissue B cells exhibit a memory-like B cell profile similar to the phenotype of aged B cells that are increased in spleen of old mice. Mechanistically, the age-induced FALC formation and adipose B cell expansion, but not B cell transcriptional program, is dependent on the Nlrp3 inflammasome. Furthermore, B cell depletion in aged mice restores lipolysis and defense against loss of core body temperature during cold stress. These data reveal that inhibiting Nlrp3-dependent B cell accumulation can be targeted to reverse metabolic impairment in aging adipose tissue. Highlights - Adipose-resident aged B cells are increased in fat-associated lymphoid clusters (FALC) - FALC formation and adipose-resident B cell expansion during aging are regulated by the Nlrp3 inflammasome - Nlrp3 and B cell depletion in aging restores lipolysis and improves cold tolerancea" @default.
- W2936918230 created "2019-04-25" @default.
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- W2936918230 date "2019-04-13" @default.
- W2936918230 modified "2023-10-06" @default.
- W2936918230 title "Aging induces Nlrp3 inflammasome dependent adipose B cell expansion to impair metabolic homeostasis" @default.
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- W2936918230 doi "https://doi.org/10.1101/607192" @default.
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