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It remains unclear whether activated inflammatory macrophages can adopt features of tissue-resident macrophages, or what mechanisms might mediate such a phenotypic conversion. Here we show that vitamin A is required for the phenotypic conversion of interleukin 4 (IL-4)-activated monocyte-derived F4/80 int CD206 + PD-L2 + MHCII + macrophages into macrophages with a tissue-resident F4/80 hi CD206 - PD-L2 - MHCII - UCP1 + phenotype in the peritoneal cavity of mice and during the formation of liver granulomas in mice infected with Schistosoma mansoni. The phenotypic conversion of F4/80 int CD206 + macrophages into F4/80 hi CD206 - macrophages was associated with almost complete remodeling of the chromatin landscape, as well as alteration of the transcriptional profiles. Vitamin A-deficient mice infected with S. mansoni had disrupted liver granuloma architecture and increased mortality, which indicates that failure to convert macrophages from the F4/80 int CD206 + phenotype to F4/80 hi CD206 - may lead to dysregulated inflammation during helminth infection.

Vitamin A mediates conversion of monocyte-derived macrophages into tissue-resident macrophages during alternative activation