Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?

Figure 3

Macrophage polarization in type 2 diabetes. Macrophage within pancreatic tissues can be switched toward different functionalities according to the environment stimuli. M2-like macrophage supports B-cell proliferation by several trophic factors like TGF-β1 which directly induce upregulation of SMAD7 and increases of cyclinD1, cyclinD2, and p27 (A). Moreover, M2-like macrophages release Wnt ligands, thus activating the Wnt signaling pathway, and β-catenin, supporting β-cell replication (B). M1-like macrophage in pancreatic tissues can secrete IL-1b, inhibiting insulin secretion, followed by islet destruction (C). Adipose-derived macrophages (ATM) can release proinflammatory cytokines, including TNF-α, IL-6, and IL-1β that decrease insulin sensitivity through the activation of Jun N-terminal kinase (JNK), inhibitor of IKκB kinase (IKK-β), and other serine kinases in insulin target cells (D).