{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Matellan C"],"funding":["Irish Research Council","Science Foundation Ireland","Irish Research Council (An Chomhairle um Thaighde in Éirinn)","Science Foundation Ireland (SFI)"],"pagination":["1958-1970"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11149899"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["212(12)"],"pubmed_abstract":["Fibroblasts acquire a proinflammatory phenotype in inflammatory bowel disease, but the factors driving this process and how fibroblasts contribute to mucosal immune responses are incompletely understood. TNF superfamily member 12 (TNFSF12, or TNF-like weak inducer of apoptosis [TWEAK]) has gained interest as a mediator of chronic inflammation. In this study, we explore its role as a driver of inflammatory responses in fibroblasts and its contribution to fibroblast-monocyte interaction using human primary colonic fibroblasts, THP-1 and primary monocytes. Recombinant human TWEAK induced the expression of cytokines, chemokines, and immune receptors in primary colonic fibroblasts. The TWEAK upregulated transcriptome shared 29% homology with a previously published transcriptional profile of inf"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["The TNFSF12/TWEAK Modulates Colonic Inflammatory Fibroblast Differentiation and Promotes Fibroblast-Monocyte Interactions."],"pmcid":["PMC11149899"],"funding_grant_id":["GOIPD/2023/1118","21/PATH-S/9621","15/IA/3152","15/US/B3130"],"pubmed_authors":["Shannon C","Santiago-Vela MI","Wu A","Aceves SS","Kennedy C","Matellan C","Ni Chathail MB","Roche HM","Manresa MC","Godson C","Hochegger J"],"additional_accession":[]},"is_claimable":false,"name":"The TNFSF12/TWEAK Modulates Colonic Inflammatory Fibroblast Differentiation and Promotes Fibroblast-Monocyte Interactions.","description":"Fibroblasts acquire a proinflammatory phenotype in inflammatory bowel disease, but the factors driving this process and how fibroblasts contribute to mucosal immune responses are incompletely understood. TNF superfamily member 12 (TNFSF12, or TNF-like weak inducer of apoptosis [TWEAK]) has gained interest as a mediator of chronic inflammation. In this study, we explore its role as a driver of inflammatory responses in fibroblasts and its contribution to fibroblast-monocyte interaction using human primary colonic fibroblasts, THP-1 and primary monocytes. Recombinant human TWEAK induced the expression of cytokines, chemokines, and immune receptors in primary colonic fibroblasts. The TWEAK upregulated transcriptome shared 29% homology with a previously published transcriptional profile of inf","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2026-06-02T06:10:41.358Z","creation":"2026-04-15T03:09:52.127Z"},"accession":"S-EPMC11149899","cross_references":{"pubmed":["38700420"],"doi":["10.4049/jimmunol.2300762"]}}