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Objectives To define stromal-immune cell crosstalk in cutaneous lupus erythematosus (CLE) using a data-driven approach.Methods We performed 3’ scRNA-seq on lesional and non-lesional skin biopsies from patients with subacute cutaneous lupus (SCLE) and healthy volunteers (HV). Cell-cell communication was interrogated by combining LIANA+ consensus analysis with tensor-cell2cell (dimensionality reduction). We interpreted biological information from interactions using gene set enrichment (Reactome) and functional enrichment (PROGENy).Results We analysed fibroblasts (FBs), monocytes, NK, and T cells from paired lesional and non-lesional samples from 3 patients and samples from 3 HV. We identified 8 cell-cell context aware factors, each representing a cell-cell communication program. Of these 3 were significantly associated with lesional samples: Factor 1 (rho=0.738, Adj.p-value=0.023), Factor 5 (rho=0.685, Adj.p-value=0.041), and Factor 8 (rho=-0.843, Adj.p-value= 0.004).Factor 1 is dominated by inflammatory signals between myeloid cells. However, Factor 1 also includes changes in collagen signalling via integrins and DDR2. Overall, fibroblasts in inflamed skin downregulate key collagens.Factor 5 comprises T cell signalling (CD8-predominant) to monocytes and fibroblasts. In CLE, there is functional enrichment of PI3K and hypoxia pathways in FBs and NKFB, JAK-STAT and TNFa in monocytes. A key interaction is between HLA on CD8 T cells and LILRB1/2 on myeloid cells, suggesting that in CLE these cells may have a regulatory role.Factor 8 shows reduced FB and monocyte signalling to T cells in CLE. In disease CD4, CD8 and NK cells show upregulation in inflammatory pathways (NKFB, JAK-STAT, TNFa). At the ligand-receptor level, there is a downregulation of the BMP pathway; BMP is important in inhibiting Th17 cell development and inducing Tregs.Conclusions We have identified changes in stromal-immune cell communication in CLE and collagen changes which may modify the composition of the extracellular matrix. Our findings suggest dysregulated fibroblast-T cell cross talk which may modulate T cell responses in the context of inflammation.