However, scRNA-seq in OVA-sensitized mouse skin or human skin with atopic dermatitis has demonstrated that several other resident cell types contribute to Th2 skin inflammation, involving signaling pathways in fibroblasts or cross talk between fibroblasts and dendritic cells.54–56 In addition, interaction between S. aureus and various myeloid cells, such as mast cells, eosinophils, and basophils, also influences Th2 inflammation.57–60 Blocking neutrophil infiltration by CXCR2 blocking antibody improved MC903-induced skin inflammation in mice,61 suggesting involvement of this cell type. The gene discussed is CXCR2; the disease is atopic eczema.