Fig. 2

WAT inflammation in T2D. In WAT affected by T2D, white adipocytes exhibit a hypertrophic phenotype and facilitate polarization of M1-type macrophages through IL-6, TNF-α, and MCP-1 secretion. Additionally, neutrophils, ILC1s, pDCs, and CD4 + T cells, including Th1 and Th17, contribute to this polarization by secreting IL-1β, IFN-γ, IFN-1, and IL-22. Conversely, eosinophils and Tregs have been shown to favor M2 macrophage polarization and suppress M1 macrophage polarization, respectively. However, presence of eosinophils and Tregs is reduced in WAT in the context of T2D. Moreover, ASCs from patients with T2D display diminished immunosuppressive capabilities, impairing their ability to support M2 macrophage polarization and restrict the proliferation of CD4 + T cells. These altered ASC functions further contribute to the enhanced proliferation of B cells, which in turn promotes an increase in Th17 cells. Abbreviation: ASCs: adipose stem cells; ILC1s: innate lymphoid cells; pDCs: plasmacytoid dendritic cells; Tregs: T regulatory lymphocytes; Th1: T helper lymphocyte 1;Th17: T helper lymphocyte 17; IL-1β: interleukin-1β; IFN-γ: interferon-γ; IFN-1: interferon-1; IL-22: interleukin-22; TNF-α: tumor necrosis factor-α; IL-6: interleukin-6