Whole biopsy studies with RNA sequencing or gene arrays elucidated the immune pathways characterizing atopic dermatitis/AD, leading to development of targeted therapeutics. However, single-cell gene profiling is key for identifying rare populations and cell-specific AD biomarkers. To classify cell types and assess transcriptomic changes in lesional/LS and nonlesional/NL skin of AD patients (n¼5) versus controls (n¼7), we performed single-cell RNAseq with 10x Genomics. We isolated 23,124, 7,035, and 10,433 cells from healthy, NL, and LS skin, respectively, capturing major cutaneous cell types. Rare cell populations were also observed, including KRT79 + keratinocytes lining upper hair follicles, PROX1 + /LYVE1lymphatic endothelial cells, and a population of CCL1 + cells unique to AD lesions, co-expressing immune, keratinocyte, and endothelial markers. LS keratinocytes had higher frequency KRT1/ 10 + cells and genomic dysregulation of hyper-proliferative keratins (KRT6A/16) and products of Th2 (CCL2/CCL27), Th17/Th22 (S100A7/8/9), and interferon (IFITM1/3). Generally, immune cells (T-cells including tissue resident memory T-cells/Trm, NK T-cells, Langerhans cells, dendritic cells/DCs, inflammatory epidermal DCs/IDECs), but not macrophages, were expanded in LS AD. LS AD T-cells had increases in Th2 (IL-13), Th22 (IL-22), and a proliferating T-cell population (MKI67). LS skin showed increases in Th2 chemokines (CCL13/ CCL17/CCL18/CCL22), mainly produced by DCs and macrophages, and in SELE, a cell adhesion gene, in vascular endothelium. A unique population of COL6A5/6 + fibroblasts, producing chemokines CCL2/CCL19, was exclusive to LS AD. Overall, scRNA-seq provides insight into AD-related cell composition and suggests that novel CCL19-producing fibroblasts might orchestrate lymphoid organization and inflammation in AD.