In contrast, moDCs treated with UVB + IFN-β–primed keratinocyte supernatants robustly upregulated key effectors of pathogenic myeloid programming, including MMP9, PDGFB, CD80, and CD86, mirroring the in vivo transcriptional profile of CD14+ MMP9+ cells found at the dermal–epidermal junction in CLE and DM lesions (Fig. 7F). The gene discussed is CD14; the disease is dermatomyositis.