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The bigger B cell picture

Nature Reviews Immunology volume 16, page 133 (2016)Cite this article

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Decades of discoveries in immunology have elucidated most of the fundamental mechanisms that control lymphocyte development and activation. Technological progress, in particular advances in multi-parameter flow cytometry and genome sequencing, has enabled immunologists to look deeper into the minutiae of immune cell stratification, fine epigenetic regulation and the cellular mechanisms that underpin fundamental immune functions. As a result, immunologists have remained for the most part 'immune-centric' and, by default, view the immune system as an autonomous and self-regulated entity that can be studied in isolation.

As I was clearing my desk a few months ago, I came across an intriguing article by Winer et al., published in 2011, that provides strong evidence that B cells have a pathogenic role in obesity-associated insulin resistance. This study looked at high fat diet (HFD)-induced obesity in mice and showed that there are larger numbers of class-switched B cells in the visceral adipose tissue of obese HFD-fed mice compared with mice fed a normal chow diet. Surprisingly, B cell-deficient mice on a HFD were protected against insulin resistance, which indicates that B cells might have a pathogenic role in obesity-dependent metabolic disease. B cells from HFD-fed mice (but not normal chow-fed mice) were pathogenic, and their pathogenicity depended on MHC class I- and MHC class II-mediated activation of CD8+ T cells and CD4+ T cells, respectively. Remarkably, the pathogenicity of HFD-induced B cell populations was mediated through the production of autoantibodies. The Fc portion of these antibodies is required to induce insulin resistance, which suggests a possible role of complement activation — as a source of pro-inflammatory signalling through complement C3 and complement receptor C3aR — in underpinning inflammation in the visceral adipose tissue.

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References

  1. Winer, D. A. et al. B cells promote insulin resistance through modulation of T cells and production of pathogenic IgG antibodies. Nat. Med. 17, 610–617 (2011)

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Authors and Affiliations

  1. School of Biomedical Sciences, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, 3010, Victoria, Australia

    Fabienne Mackay

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  1. Fabienne Mackay
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Correspondence to Fabienne Mackay.

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DeFuria, J. et al. B cells promote inflammation in obesity and type 2 diabetes through regulation of T-cell function and an inflammatory cytokine profile. Proc. Natl Acad. Sci. USA 110, 5133–5138 (2013)

Nishimura,S.etal.AdiposenaturalregulatoryBcellsnegativelycontroladiposetissueinflammation.CellMetab.http://dx.doi.org/10.1016/j.cmet.2013.09.017(2013)

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Mackay, F. The bigger B cell picture. Nat Rev Immunol 16, 133 (2016). https://doi.org/10.1038/nri.2016.3

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