An anti-obesity immunotherapy?

Adipose tissue–resident macrophages promote lipid storage in mice but can be stopped with antibody treatment Energy storage is a crucial physiological process for all metazoans, the mechanisms of which are at least partially conserved across the animal kingdom. Lipid-storing adipocytes, the major constituent cell type of adipose tissues, are specialized for the storage of energy in the form of lipid triglycerides. Macrophages are an evolutionarily conserved immune cell population and are the most abundant immunocyte in obese adipose tissue. Recruited monocyte-derived macrophages have long been implicated in promoting the adipose tissue inflammation and metabolic diseases associated with obesity. However, a defined role for adipose tissue–resident macrophages in energy storage has remained elusive. On page 74 of this issue, Cox et al. ( 1 ) demonstrate that adipose-resident macrophages—through a conserved mechanism—directly regulate energy storage in adipocytes through the mammalian platelet-derived growth factor PDGFc and its Drosophila melanogaster ortholog, PDGF- and VEGF-related factor 3 ( Pvf3 ). This study introduces a new, macrophage-centered paradigm in metazoan energy storage.