Metabolic regulation and immune signaling areclosely linked, as evidenced by both thephysical proximity between metabolic cells(e.g., adipocytes and hepatocytes) and resident macrophages as well as the progression of inflammation in metabolic syndrome. Contrasting the reactions to pathogen infections, meta-inflammation describes a novel type of low-grade, unresolvable immune response that is in the causal pathway to metabolic dysregulation (1). Although howmeta-inflammation is initiated remains unclear, the T-helper cell type 1 (Th1)/Th2 (or M1/M2) paradigm provides a simplified view of how immune cells are involved in readjusting metabolic set points in response to nutrient intake (2). It appears that Th1 cytokines (e.g., interleukin [IL]-12 and interferon-g [IFNg]) or Th1 polarized immune cells pro-mote insulin resistance, whereas Th2 signaling (e.g., IL-4 and IL-13) sustains metabolic homeostasis (3). In mouse genetic models, for example, tipping the Th1/Th2 balanc
