Circulating monocytes are recruited to sites of inflammation, where they can acquire distinct phenotypes depending on the cytokines present within the lesion. A recent study shows that in allergic skin lesions, inflammatory monocytes interact with basophils and adopt an M2-like phenotype, which is associated with anti-inflammatory functions (Immunity 38, 570–580, 2013).

Credit: Michel Gilles / Science Source

Hajime Karasuyama and his colleagues report that in a mouse model of allergic skin inflammation, inflammatory monocytes expressing chemokine receptor 2 (CCR2) infiltrate the skin. When compared to wild-type mice, allergic inflammation is worsened and monocyte recruitment is impaired in mice deficient in CCR2, suggesting that these cells are anti-inflammatory. Once recruited to the skin, CCR2-expressing monocytes adopt an M2-like phenotype. In particular, interleukin-4 (IL-4) secreted from basophils promotes this differentiation, as IL-4R–deficient monocytes failed to upregulate M2 markers and did not suppress allergic inflammation. Although the mechanism whereby M2-type macrophages suppress allergic inflammation remains unclear, this study highlights a previously uncharacterized means whereby monocytes can differentiate into an M2-like phenotype in tissues.