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B Lymphocytes in the Adipose Tissue Microenvironment: Multifaceted Roles in Inflammation and Metabolic Dysfunction
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DOI：10.1111/imm.70178.png)
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Abstract
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Adipose tissue (AT) is now recognised as a dynamic immunometabolic organ in which coordinated interactions between adipocytes, stromal cells, vascular elements, and resident immune populations are essential for maintaining metabolic homeostasis and endocrine function. Beyond its classical role in energy storage, AT actively regulates local and systemic immune responses through the production of adipokines, cytokines, chemokines, and lipid mediators. Among adipose-resident immune cells, B lymphocytes have emerged as multifaceted regulators of tissue inflammation, remodelling, and metabolic function. Distinct B cell subsets populate adipose depots and exert diverse activities, including antibody production, cytokine secretion, antigen presentation, and modulation of innate and adaptive immune responses. In obesity, aging, and chronic inflammatory conditions, AT undergoes profound immunological remodelling characterised by altered adipokine signalling, inflammasome activation, recruitment of inflammatory immune cells, and production of pathogenic autoantibodies. Conventional B-2 cells, double-negative B cells, and T-bet+ age-associated B cells generally promote inflammatory responses and insulin resistance through secretion of pro-inflammatory cytokines and IgG autoantibodies, whereas regulatory B cells and innate-like B-1 cells exert protective effects through IL-10 production and natural IgM antibodies. This review summarises current knowledge regarding the development, localisation, and functional specialisation of AT-resident B cell populations and examines the molecular mechanisms governing adipocyte–B cell crosstalk, including adipokine signalling, chemokine-mediated migration, antigen presentation, and inflammasome-associated pathways. It further discusses how dysregulation of these interactions contributes to metabolic inflammation, autoimmunity, and AT remodelling, and highlights emerging therapeutic strategies targeting B cell signalling and trafficking pathways in obesity-associated metabolic disease.
Keywords:
adaptive immunity
aging
B cell
damage-associated molecular patterns (DAMPs)
diabetes
inflammasome
innate immunity
obesity
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