{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li TM"],"funding":["Barbara Volcker Center for Women and Rheumatic Diseases","BLRD VA","NIH MSTP grant","NIAID NIH HHS","Erwin Schrodinger Fellowship","Alpha Omega Alpha Honor Medical Society Carolyn L. Kuckein fellowship","Lupus Research Alliance","Veterans Administration VA Merit","NIH","St. Giles Foundation","HSS Medical Student Summer Research Fellowhship","Dermatology Foundation Physician Scientist Career Development Award","NIDDK NIH HHS","DOD","NIAMS NIH HHS","Tow Foundation","NIH HHS","NIGMS NIH HHS","A Lasting Mark Foundation"],"pagination":["e85914"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11213570"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13"],"pubmed_abstract":["The autoimmune disease lupus erythematosus (lupus) is characterized by photosensitivity, where even ambient ultraviolet radiation (UVR) exposure can lead to development of inflammatory skin lesions. We have previously shown that Langerhans cells (LCs) limit keratinocyte apoptosis and photosensitivity via a disintegrin and metalloprotease 17 (ADAM17)-mediated release of epidermal growth factor receptor (EGFR) ligands and that LC ADAM17 sheddase activity is reduced in lupus. Here, we sought to understand how the lupus skin environment contributes to LC ADAM17 dysfunction and, in the process, differentiate between effects on LC ADAM17 sheddase function, LC ADAM17 expression, and LC numbers. We show through transcriptomic analysis a shared IFN-rich environment in non-lesional skin across human"],"journal":["eLife"],"pubmed_title":["The interferon-rich skin environment regulates Langerhans cell ADAM17 to promote photosensitivity in lupus."],"pmcid":["PMC11213570"],"funding_grant_id":["T32 GM007739","R01 AR077194","I01 BX004907","R01AI079178","W81XWH-21-LRP-IPA","R01 AR080436","R21 AR081493","R35GM134907","S10 OD019986","DK099087","K08 AR069111","R35 GM134907","T32AR071302","R01AR077194","R01 AI079178","J 4638-B FWF","T32 AR071302","T32GM007739","R01 DK099087"],"pubmed_authors":["Jabbari A","Li TM","Oliver DJ","Veiga KR","Taber SF","Rogatsky I","Liu Y","Onel KB","Shipman WD","Seltzer ES","Zippin JH","Chinenov Y","Blobel CP","Rashighi M","Cabahug-Zuckerman P","Zyulina V","Daamen AR","Krueger JG","Schwartz N","Lu TT","Lipsky PE","Anandasabapathy N","Ambler WG","Lora J","Dacic M"],"additional_accession":[]},"is_claimable":false,"name":"The interferon-rich skin environment regulates Langerhans cell ADAM17 to promote photosensitivity in lupus.","description":"The autoimmune disease lupus erythematosus (lupus) is characterized by photosensitivity, where even ambient ultraviolet radiation (UVR) exposure can lead to development of inflammatory skin lesions. We have previously shown that Langerhans cells (LCs) limit keratinocyte apoptosis and photosensitivity via a disintegrin and metalloprotease 17 (ADAM17)-mediated release of epidermal growth factor receptor (EGFR) ligands and that LC ADAM17 sheddase activity is reduced in lupus. Here, we sought to understand how the lupus skin environment contributes to LC ADAM17 dysfunction and, in the process, differentiate between effects on LC ADAM17 sheddase function, LC ADAM17 expression, and LC numbers. We show through transcriptomic analysis a shared IFN-rich environment in non-lesional skin across human","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-06-01T05:51:29.455Z","creation":"2026-04-08T09:45:41.146Z"},"accession":"S-EPMC11213570","cross_references":{"pubmed":["38860651"],"doi":["10.7554/eLife.85914"]}}