Non-lesional lupus skin contributes to inflammatory education of myeloid cells and primes for cutaneous inflammation
dc.contributor.author | Billi, AC | |
dc.contributor.author | Ma, F | |
dc.contributor.author | Plazyo, O | |
dc.contributor.author | Gharaee-Kermani, M | |
dc.contributor.author | Wasikowski, R | |
dc.contributor.author | Hile, GA | |
dc.contributor.author | Xing, X | |
dc.contributor.author | Yee, CM | |
dc.contributor.author | Rizvi, SM | |
dc.contributor.author | Maz, MP | |
dc.contributor.author | Berthier, CC | |
dc.contributor.author | Wen, F | |
dc.contributor.author | Tsoi, LC | |
dc.contributor.author | Pellegrini, M | |
dc.contributor.author | Modlin, RL | |
dc.contributor.author | Gudjonsson, JE | |
dc.contributor.author | Kahlenberg, JM | |
dc.coverage.spatial | United States | |
dc.date.accessioned | 2024-02-03T15:31:18Z | |
dc.date.available | 2024-02-03T15:31:18Z | |
dc.date.issued | 2021-11-01 | |
dc.identifier.issn | 1946-6234 | |
dc.identifier.issn | 1946-6242 | |
dc.identifier.uri | https://www.ncbi.nlm.nih.gov/pubmed/35476593 | |
dc.identifier.uri | https://hdl.handle.net/2027.42/192260 | en |
dc.description.abstract | Cutaneous lupus erythematosus (CLE) is a disfiguring and poorly understood condition frequently associated with systemic lupus. Previous studies suggest that nonlesional keratinocytes play a role in disease predisposition, but this has not been investigated in a comprehensive manner or in the context of other cell populations. To investigate CLE immunopathogenesis, normal-appearing skin, lesional skin, and circulating immune cells from lupus patients were analyzed via integrated single-cell RNA sequencing and spatial RNA sequencing. We demonstrate that normal-appearing skin of patients with lupus represents a type I interferon–rich, prelesional environment that skews gene transcription in all major skin cell types and markedly distorts predicted cell-cell communication networks. We also show that lupus-enriched CD16+ dendritic cells undergo robust interferon education in the skin, thereby gaining proinflammatory phenotypes. Together, our data provide a comprehensive characterization of lesional and nonlesional skin in lupus and suggest a role for skin education of CD16+ dendritic cells in CLE pathogenesis. | |
dc.format.medium | Print-Electronic | |
dc.language | eng | |
dc.publisher | American Association for the Advancement of Science (AAAS) | |
dc.relation.haspart | ARTN eabn2263 | |
dc.subject | Humans | |
dc.subject | Inflammation | |
dc.subject | Interferon Type I | |
dc.subject | Keratinocytes | |
dc.subject | Lupus Erythematosus, Cutaneous | |
dc.subject | Myeloid Cells | |
dc.title | Non-lesional lupus skin contributes to inflammatory education of myeloid cells and primes for cutaneous inflammation | |
dc.type | Article | |
dc.identifier.pmid | 35476593 | |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/192260/2/Nonlesional lupus skin contributes to inflammatory education of myeloid cells and primes for cutaneous inflammation.pdf | |
dc.identifier.doi | 10.1126/scitranslmed.abn2263 | |
dc.identifier.doi | https://dx.doi.org/10.7302/22169 | |
dc.identifier.source | Sc. Transl. Med | |
dc.description.version | Published version | |
dc.date.updated | 2024-02-03T15:31:14Z | |
dc.identifier.orcid | 0000-0001-7115-9113 | |
dc.identifier.orcid | 0000-0002-6859-7590 | |
dc.identifier.orcid | 0000-0002-2177-2427 | |
dc.identifier.orcid | 0000-0003-3539-1075 | |
dc.identifier.orcid | 0000-0001-7970-4796 | |
dc.identifier.orcid | 0000-0003-1627-5722 | |
dc.identifier.orcid | 0000-0002-0080-0812 | |
dc.identifier.orcid | 0000-0002-4006-8945 | |
dc.identifier.volume | 14 | |
dc.identifier.issue | 642 | |
dc.identifier.startpage | eabn2263 | |
dc.identifier.name-orcid | Billi, AC; 0000-0001-7115-9113 | |
dc.identifier.name-orcid | Ma, F | |
dc.identifier.name-orcid | Plazyo, O; 0000-0002-6859-7590 | |
dc.identifier.name-orcid | Gharaee-Kermani, M; 0000-0002-2177-2427 | |
dc.identifier.name-orcid | Wasikowski, R | |
dc.identifier.name-orcid | Hile, GA | |
dc.identifier.name-orcid | Xing, X | |
dc.identifier.name-orcid | Yee, CM | |
dc.identifier.name-orcid | Rizvi, SM | |
dc.identifier.name-orcid | Maz, MP | |
dc.identifier.name-orcid | Berthier, CC; 0000-0003-3539-1075 | |
dc.identifier.name-orcid | Wen, F; 0000-0001-7970-4796 | |
dc.identifier.name-orcid | Tsoi, LC; 0000-0003-1627-5722 | |
dc.identifier.name-orcid | Pellegrini, M | |
dc.identifier.name-orcid | Modlin, RL | |
dc.identifier.name-orcid | Gudjonsson, JE; 0000-0002-0080-0812 | |
dc.identifier.name-orcid | Kahlenberg, JM; 0000-0002-4006-8945 | |
dc.working.doi | 10.7302/22169 | en |
dc.owningcollname | Internal Medicine, Department of |
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