Basophils play critical roles in the development of delayed-onset skin allergic inflammation in mice (IgE-CAI model). Importantly, they also contribute to the resolution of allergic inflammation by promoting the generation of M2 macrophages. However, it remains unclear how M2 macrophages suppress excess inflammation. To address this, we conducted single-cell RNA-seq (scRNA-seq) analysis of the IgE-CAI skin lesion. scRNA-seq analysis identified two distinct M2 macrophage populations, namely early and late M2 macrophages, in IgE-CAI skin lesion. The former population was preferentially observed at the peak of inflammation (3 days after allergen challenge), whereas the latter one at the termination phase of inflammation (5 days). Gene ontology analysis revealed that genes associated with phagocytosis were enriched in late M2 macrophages. In particular, late M2 macrophages displayed upregulated expression of Gas6 and Mertk, key genes responsible for phagocytic clearance of apoptotic cells. Of note, MERTK inhibitor significantly aggravated ear swelling and accumulation of inflammatory cells in the skin lesion. Taken together, scRNA-seq identified M2 macrophages that display high capacity of dead cell clearance and contribute to the resolution of IgE-CAI.