Extended Data Fig. 9: pDC fate-switching during skin inflammation.

a-f, CITE-seq analysis of healthy and inflamed human skin samples from a public dataset⁴³. a, RNA UMAP of myeloid cell clusters (subsetted based on positive HLA-DR⁺ and MS4A1⁻ gene expression). ‘HSP-myeloid’ denotes a myeloid cell cluster with high heat-shock protein expression, ‘LC’ denotes Langerhans cells. ‘cDC2act’ denotes an activated cDC2 cluster. b-c, Expression of key critical transcriptional (b) or protein (c) markers distinguishing cellular clusters in (a). d, RNA UMAPs from (a), showing cellular distribution in: healthy controls, all inflamed lesions (atopic dermatitis, psoriasis vulgaris, bullous pemphigoid, lichen planus and patients with clinicopathologically indeterminate rash), atopic dermatitis alone, and psoriasis vulgaris alone. Numbers of donors is indicated in brackets. The pDC cluster is highlighted in blue. e, Gene signature score of DC subsets from the panDC snMultiome (top) and SMART-seq2 (bottom) datasets projected onto pDC, cDC2 and cDC2act clusters from (a). f, Heatmap of selected genes shown in (e). g, pDC conversion was analyzed in human skin blisters challenged with saline or house dust mite (HDM)⁴⁴. Shown is the “IFNα response” signature MSigDB score in CD123^hi pDCs (blue) and CD123^int DCs (orange) from saline and HDM blisters (Fig. 5a-d). h, Gene signature score of DC subsets from the panDC snMultiome dataset projected onto the saline-treated blister dataset. i, Within the HDM-treated blister dataset, CD123^hi cells were stratified onto ‘High’, ‘Middle’ and ‘Low’ groups based on panDC-pDC signature score.