AGING INDUCES NLRP3 INFLAMMASOME DEPENDENT ADIPOSE B CELL EXPANSION TO IMPAIR METABOLIC HOMEOSTASIS
2019
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
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