The effects of diet-induced obesity on B cell function

Authors

  • S. R. Shaikh,

    Corresponding author
    1. Department of Biochemistry and Molecular Biology, East Carolina Diabetes and Obesity Institute, East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, NC, USA
    2. Department of Microbiology and Immunology, East Carolina Diabetes and Obesity Institute, East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, NC, USA
    • Correspondence: S. R. Shaikh, Departments of Biochemistry and Molecular Biology, East Carolina Diabetes and Obesity Institute, East Carolina Heart Institute, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC 27834, USA.

      E-mail: shaikhsa@ecu.edu

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  • K. M. Haas,

    1. Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
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  • M. A. Beck,

    1. Department of Nutrition, Gillings School of Global Public Health, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
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  • H. Teague

    1. Department of Biochemistry and Molecular Biology, East Carolina Diabetes and Obesity Institute, East Carolina Heart Institute, Brody School of Medicine, East Carolina University, Greenville, NC, USA
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Summary

B-1 and B-2 B cell subsets carry out a diverse array of functions that range broadly from responding to innate stimuli, antigen presentation, cytokine secretion and antibody production. In this review, we first cover the functional roles of the major murine B cell subsets. We then highlight emerging evidence, primarily in preclinical rodent studies, to show that select B cell subsets are a therapeutic target in obesity and its associated co-morbidities. High fat diets promote accumulation of select murine B cell phenotypes in visceral adipose tissue. As a consequence, B cells exacerbate inflammation and thereby insulin sensitivity through the production of autoantibodies and via cross-talk with select adipose resident macrophages, CD4+ and CD8+ T cells. In contrast, interleukin (IL)-10-secreting regulatory B cells counteract the proinflammatory profile and improve glucose sensitivity. We subsequently review data from rodent studies that show pharmacological supplementation of obesogenic diets with long chain n-3 polyunsaturated fatty acids or specialized pro-resolving lipid mediators synthesized from endogenous n-3 polyunsaturated fatty acids boost B cell activation and antibody production. This may have potential benefits for improving inflammation in addition to combating the increased risk of viral infection that is an associated complication of obesity and type II diabetes. Finally, we propose potential underlying mechanisms throughout the review by which B cell activity could be differentially regulated in response to high fat diets.

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