Abstract
Alterations in macrophage activation in adipose tissue are associated with metabolic disease. In lean mice and humans, macrophages with an immunoregulatory phenotype (termed alternatively activated macrophages, or AAMs) predominate, whereas AAM numbers decrease and the numbers of proinflammatory macrophages increase when metabolic control is lost. Wu et al. (p. [243][1], published online 24 March; see the Perspective by [ Maizels and Allen ][2]) now show that eosinophils, an immune cell type classically associated with parasitic infections and allergy, regulate the number of AAMs present in adipose tissue in mice. Eosinophils were detected in adipose tissue where they produced interleukin-4, a cytokine that promotes the AAM phenotype. Eosinophil deficiency in mice was associated with a decrease in AAMs in adipose tissue and increased body fat and blood glucose levels in mice fed a high-fat diet. In contrast, genetic or parasite-induced increases in eosinophil numbers resulted in improved metabolic read-outs in mice fed a high-fat diet. [1]: /lookup/volpage/332/243 [2]: /lookup/volpage/332/186?iss=6026
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