<HashMap><database>biostudies-literature</database><scores/><additional><submitter>He G</submitter><funding>Natural Science Foundation of Henan Province (Henan Province Natural Science Foundation)</funding><funding>China Postdoctoral Science Foundation</funding><funding>National Natural Science Foundation of China (National Science Foundation of China)</funding><pagination>395</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11890729</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><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 </pubmed_abstract><journal>Communications biology</journal><pubmed_title>Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis.</pubmed_title><pmcid>PMC11890729</pmcid><funding_grant_id>811900024</funding_grant_id><funding_grant_id>232300421180</funding_grant_id><funding_grant_id>2019M662542, 2020T130606</funding_grant_id><pubmed_authors>Luan Y</pubmed_authors><pubmed_authors>Yang J</pubmed_authors><pubmed_authors>Zheng H</pubmed_authors><pubmed_authors>Wang P</pubmed_authors><pubmed_authors>Yang K</pubmed_authors><pubmed_authors>He G</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Liu P</pubmed_authors><pubmed_authors>Xuan X</pubmed_authors><pubmed_authors>Zhang M</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Yang Q</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis.</name><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 </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2025-04-04T08:22:57.334Z</modification><creation>2025-04-04T08:22:57.334Z</creation></dates><accession>S-EPMC11890729</accession><cross_references><pubmed>40057592</pubmed><doi>10.1038/s42003-025-07742-4</doi></cross_references></HashMap>