Abstract
In atopic dermatitis (AD), skin barrier and immune dysfunction result in chronic tissue inflammation, yet our understanding of the tissue ecosystem remains incomplete. Here, we generate a multi-modal census of 280,518 cells from whole skin tissue samples from 17 adults, including 11 AD patients, integrating it with 430,186 cell profiles from four previous studies into a comprehensive human skin cell atlas. Reconstruction of keratinocyte differentiation revealed disrupted cornification in AD associated with signals from an immune and stromal multicellular community – comprising MMP12+ and migratory dendritic cells (DCs), cycling innate lymphoid cells (ILC), natural killer cells, inflammatory CCL19+ IL4I1+ fibroblasts, and clonally expanded IL13+IL22+IL26+ T cells connected by intercellular feedback loops predicted to impact community assembly. Subsets from this community, along with disrupted cornified keratinocytes, were enriched in GWAS, suggesting that dysfunction in this communication network may initiate AD. Our work highlights disease-associated cell subsets and interactions in chronic skin inflammation.
Data availability
Data associated with this work are available at the Gene Expression Omnibus (GEO) under accession GSE204765. Raw fastq files for adult samples are deposited on dbGAP as controlled access data under accession phs004337.v1.p1 (https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs004337.v1.p1). Raw fastq files for pediatric samples cannot be deposited in a public repository because of restrictions in the informed consent, and may be requested from L.S. (Lynda.Schneider@childrens.harvard.edu). Dr. Schneider will respond to requests within 2 weeks; access to data will be granted after individuals are added to the IRB, and appropriate institutional approvals will typically be completed within 2 months. Processed scRNA-seq data of the current study and the curated Atopic Dermatitis Atlas are available at https://cellxgene.cziscience.com/collections/5e143645-177c-45b6-952d-48770e29a54b, https://singlecell.broadinstitute.org/single_cell/study/SCP2613, and https://singlecell.broadinstitute.org/single_cell/study/SCP2738. The scleroderma data and the mmDCs from our AD study and public studies are available at https://singlecell.broadinstitute.org/single_cell/study/SCP3122 and https://singlecell.broadinstitute.org/single_cell/study/SCP3120, respectively. The 5′-scRNA-Seq + scTCR-Seq dataset is available at https://singlecell.broadinstitute.org/single_cell/study/SCP3036. Source data are provided with this paper.
Code availability
Code for all analyses is available on GitHub: https://doi.org/10.5281/zenodo.17211367.
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Acknowledgements
The authors thank members of the Regev, Xavier, and Geha laboratories for helpful discussions. The authors thank L. Gaffney, A. Hupalowska, H. Kang, and S. Aldrich for help with figure preparation and E. Heppenheimer for critical reading of the manuscript. This research was supported by NHGRI grants 5RM1 HG006193 (Center for Cell Circuits, to A.R.), Klarman Cell Observatory (A.R., R.J.X.), DK043351 and DK114784 (to R.J.X.), NIAID/NIH grant 1UM1AI151958 (to R.S.G.), and a gift from the Food Allergy Science Initiative (to A.R. and R.J.X.), a gift from the Manton Foundation (to A.R. and R.J.X.), and HHMI (to A.R.). E.F. is supported by an EMBO Long-Term fellowship, J.M.L.-C. by NIAID T32 grant (5T32AI007512-32), NIH award (UL1 TR002541), and a Dermatology Foundation Career Development Award. C.A.L. is supported by a Stanford Science Fellowship. A.R. was a Howard Hughes Medical Institute Investigator (until July 31, 2020). This paper is part of the Human Cell Atlas.
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E.F., G.E., O.R.-R., R.S.G., R.J.X., and A.R. conceived and designed the project. E.F. designed and performed experiments. E.F., G.E., O.A., T.J., J.D., and T.M.D. analyzed and interpreted the data, with guidance from A.R. G.E. designed and led data analysis, with guidance from A.R. M.B.A.-P. performed clinical work. C.A.L. contributed to data analysis. E.F., M.B.A.-P., J.M.L.-C. collected biopsies, E.P.F. and I.T.-S. performed additional tissue processing and scRNA-seq experiments. E.F., S.I. performed mouse MC903 experiments. M.S., J.W., and T.M.D. provided experimental assistance. H.C., S.K., H.L., B.L., A.C., B.W., W.P., L.S., C.P., and J.C. assisted in patient recruitment and biopsy collection. G.P.S., T.M.D., J.D., O.R.-R., R.S.G., R.J.X., and A.R. provided project oversight and acquired funding. E.F., G.E., O.A., T.J., T.M.D., R.J.X., and A.R. wrote the manuscript with input from all authors.
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A.R. was a founder and equity holder of Celsius Therapeutics, is an equity holder in Immunitas Therapeutics, and until 31 July 2020 was an SAB member of Syros Pharmaceuticals, Neogene Therapeutics, Asimov, and ThermoFisher Scientific. From 1 August 2020, A.R. is an employee of Genentech, a member of the Roche Group, with equity in Roche. R.J.X. is a co-founder of Celsius Therapeutics, Jnana Therapeutics, and director of Moonlake Immunotherapeutics. R.J.X. is an SAB member of Magnet Biomedicine and of Nestlé. From 19 October 2020 to 4 April 2022, respectively, O.R.-R. and G.E. are employees of Genentech, a member of the Roche Group, and have equity in Roche. The remaining authors declare no competing interests.
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Fiskin, E., Eraslan, G., Alora-Palli, M.B. et al. Multi-modal skin atlas identifies a multicellular immune-stromal community associated with disrupted cornification and specific T cell expansion in atopic dermatitis. Nat Commun (2026). https://doi.org/10.1038/s41467-026-69587-7
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DOI: https://doi.org/10.1038/s41467-026-69587-7
