Interplay between the immune system and adipose tissue in obesity

  1. Lydia Lynch4
  1. 1Department of Medicine, Brigham and Women's Hospital, Thorn Bldg, 1405, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
    2Faculty of Medical and Human Sciences, Manchester Collaborative Centre for Inflammation Research (MCCIR), University of Manchester, 46 Grafton Street, CTF Building Room 2.14b, Manchester M13 9NT, UK
    3Department of Endocrinology, St. Vincent's University Hospital, University College Dublin, Dublin, Ireland
    4Department of Medicine, Brigham and Women's Hospital, Smith Building, Harvard Medical School, One Jimmy Fund Way, Boston, Massachusetts 02115, USA
  1. Correspondence should be addressed to M A Exley; Email: mexley{at}
  1. Figure 1

    Adipose homeostasis during steady-state and obese conditions. In lean adipose tissue, immune cells and adipocytes are neighbors and interact to maintain homeostasis and regulation of adipocyte lipid handling and storage. The main resident immune cells include iNKT cells, Tregs, eosinophils, IgM-producing B cells, and alternatively activated M2 macrophages. IL10 production by iNKT, Tregs, and M2 macrophages, and IL4 production by eosinophils is important for maintaining a tolerogenic environment. During adipose expansion in obesity, there is a loss of iNKT cells and Tregs, and a phenotypic switch in macrophages from M2 to M1, which accumulate around overloaded and rupturing adipocytes.

  2. Figure 2

    iNKT cells and macrophages are important gatekeepers of adipose homeostasis. During steady state, anti-inflammatory iNKT cells accumulate in adipose tissue and produce IL10, which regulates macrophage M2 phenotype and adipocyte insulin sensitivity. M2 macrophages are also a source of IL10, propagating a tolerogenic environment. In obesity, the loss of iNKT cells results in decreased adipose IL10, which may play a role in macrophage polarization to an anti-inflammatory state. Accumulation of M1 macrophages is probably beneficial to ‘mopping up’ excess lipids from overloaded adipocytes. However, their chronic activation and production of pro-inflammatory cytokines lead to a vicious cycle, resulting in insulin resistance in adipose tissue and increased circulating pro-inflammatory markers. Adipose lipid spillover can relocate to liver and, in concert with increased systemic inflammation, leads to peripheral insulin resistance.

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  1. J Endocrinol 223 R41-R48
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