{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["He G"],"funding":["Natural Science Foundation of Henan Province (Henan Province Natural Science Foundation)","China Postdoctoral Science Foundation","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["395"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11890729"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(1)"],"pubmed_abstract":["Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting disease characterized by chronic inflammation in the gastrointestinal tract. The exact etiology and pathogenesis of IBD remain elusive. Although ELF-1 has been known to be highly expressed in epithelial cells for past twenty years, little is known about its function in epithelial cells and epithelial-related IBD. Here, we demonstrated that ELF-1 deficiency in mouse lead to exacerbated DSS-induced colitis, marked by inflammation dominated by neutrophil infiltration and activation of IL-17 signaling pathways in various immune cells, including Th17, ILC3, γδT and NKT cells. Bone marrow transfer experiments confirmed ELF-1 deficiency in non-hematopoietic cells intrinsically worsened DSS-induced colitis. On one hand, ELF-1 "],"journal":["Communications biology"],"pubmed_title":["Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis."],"pmcid":["PMC11890729"],"funding_grant_id":["811900024","232300421180","2019M662542, 2020T130606"],"pubmed_authors":["Luan Y","Yang J","Zheng H","Wang P","Yang K","He G","Zhang H","Liu P","Xuan X","Zhang M","Li Q","Yang Q"],"additional_accession":[]},"is_claimable":false,"name":"Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis.","description":"Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting disease characterized by chronic inflammation in the gastrointestinal tract. The exact etiology and pathogenesis of IBD remain elusive. Although ELF-1 has been known to be highly expressed in epithelial cells for past twenty years, little is known about its function in epithelial cells and epithelial-related IBD. Here, we demonstrated that ELF-1 deficiency in mouse lead to exacerbated DSS-induced colitis, marked by inflammation dominated by neutrophil infiltration and activation of IL-17 signaling pathways in various immune cells, including Th17, ILC3, γδT and NKT cells. Bone marrow transfer experiments confirmed ELF-1 deficiency in non-hematopoietic cells intrinsically worsened DSS-induced colitis. On one hand, ELF-1 ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-04-04T08:22:57.334Z","creation":"2025-04-04T08:22:57.334Z"},"accession":"S-EPMC11890729","cross_references":{"pubmed":["40057592"],"doi":["10.1038/s42003-025-07742-4"]}}