Figure 1
Leukocyte subsets present in WAT. (A) In lean individuals, eosinophils, innate lymphoid type 2 cells (ILC2s), and type I (or invariant) natural killer T (iNKT) cells support activation of alternatively activated (M2) macrophages, which secrete interleukin-10 (IL-10) to promote insulin sensitivity, while regulatory T cells (Treg’s) secrete IL-10, which contributes to M2 activation and directly promotes insulin sensitivity. In obese individuals, CD8+ and CD4+-Th1 T cells secrete proinflammatory cytokines that sustain inflammatory macrophage production of TNF-α, IL-1β, and IL-6 to promote insulin resistance. Neutrophils, mast cells, and B cells also infiltrate the obese adipose tissue and contribute to the inflammatory microenvironment. (B) Schematic representation of weight gain–induced changes in the WAT leukocyte population. IFN-γ, interferon γ; M1, classically activated; Th, T helper.

Leukocyte subsets present in WAT. (A) In lean individuals, eosinophils, innate lymphoid type 2 cells (ILC2s), and type I (or invariant) natural killer T (iNKT) cells support activation of alternatively activated (M2) macrophages, which secrete interleukin-10 (IL-10) to promote insulin sensitivity, while regulatory T cells (Treg’s) secrete IL-10, which contributes to M2 activation and directly promotes insulin sensitivity. In obese individuals, CD8+ and CD4+-Th1 T cells secrete proinflammatory cytokines that sustain inflammatory macrophage production of TNF-α, IL-1β, and IL-6 to promote insulin resistance. Neutrophils, mast cells, and B cells also infiltrate the obese adipose tissue and contribute to the inflammatory microenvironment. (B) Schematic representation of weight gain–induced changes in the WAT leukocyte population. IFN-γ, interferon γ; M1, classically activated; Th, T helper.

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