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Comment
. 2020;2(2):e200011.
doi: 10.20900/immunometab20200011. Epub 2020 Feb 18.

Commentary on Camell et al., Aging Induces Nlrp3 Inflammasome Dependent Adipose B Cell Expansion to Impair Metabolic Homeostasis

Sara SantaCruz-Calvo  1 , Lucia SantaCruz-Calvo  2 , Barbara S Nikolajczyk  1
Affiliations
Comment

Commentary on Camell et al., Aging Induces Nlrp3 Inflammasome Dependent Adipose B Cell Expansion to Impair Metabolic Homeostasis

Sara SantaCruz-Calvo et al. Immunometabolism. 2020.

Abstract

The burden of aging and obesity is urging extended investigation into the molecular mechanisms that underlie chronic adipose tissue inflammation. B cell-targeted therapies are emerging as novel tools to modulate the immune system and thereby mitigate aging and obesity-related metabolic complications.

Keywords: B cells; FALC; adipose tissue; aging; inflammation; obesity.

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Conflict of interest statement

CONFLICTS OF INTEREST The authors declare that there are no conflicts of interest.

Figures

Figure 1.
Figure 1.
(A) Schematic representation of possible differences in VAT-resident immune cells (blue: AAB, green: macrophages, pink: Treg, teal: Breg; couls also be B1-a), pro-inflammatory cytokines (yellow: IL-1β, dark blue IL-18), anti-inflammatory cytokine (teal: IL-10) and leptin (purple) levels secreted by the adipocytes in young and aged-VAT-FALCS. (B) Schematic representation of some of the key players involved in the expansion of AAB in aged-VAT-FALCS showing the activation of the NLP3 inflammasome, caspase 1, IL-1β receptor (IL-1βR) and the possible activation of leptin receptor (LepR).
See this image and copyright information in PMC

Comment on

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