Figure 3 Regulation of insulin sensitivity by innate immune cells

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Figure 3 Regulation of insulin sensitivity by innate immune cells Figure 3 | Regulation of insulin sensitivity by innate immune cells. a | Promotion of insulin sensitivity in the lean state. IL-33 induces group 2 innate lymphoid cells (ILC2) to produce IL-5 and IL-13, supporting eosinophil chemotaxis and maintenance. Eosinophils produce IL-4 to maintain adipose tissue macrophages (ATMs) in an alternatively activated macrophage (AAM) state. AAM by-products (for example, IL-10) promote adipocyte insulin sensitivity. IL-4 primes beige adipocyte precursor cells for subsequent beiging signals, such as catecholamines and methionine-enkephalin peptides (MetEnk). The invariant T-cell receptor on invariant natural killer T (iNKT) cells binds glycolipid antigens presented in CD1d on the surface of ATMs and adipocytes. b | Promotion of insulin resistance in the obese state. Adipocytes produce chemokines, such as MCP-1, in response to proinflammatory signals (for example, tumour necrosis factor or free fatty acids) causing monocytes to migrate from the circulation into adipose tissue, differentiate into ATMs and polarize to proinflammatory classically activated macrophages (CAMs). CAMs produce proinflammatory cytokines that impair the insulin signalling pathway and chemokines that promote further CAM accumulation. Activated natural killer (NK) cells produce IFN-γ, polarizing ATMs to CAMs. Lackey, D. E. & OlefskyI, J. M. (2015) Regulation of metabolism by the innate immune system Nat. Rev. Endocrinol. doi:10.1038/nrendo.2015.189