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TWEAK is increased in ulcerative colitis and contributes to fibroblast-mediated monocyte activation via heterologous non-canonical NF-kB/STAT3 signalling

2025-09-25

Abstract excerpt

<h4>ABSTRACT</h4> <h4>Background and Aims</h4> Interactions between fibroblasts and monocytes have emerged as a contributing factor in IBD pathogenesis and therapy resistance, owing to the ability of both cell types to participate in tissue inflammation and repair. We have previously shown that the TNF superfamily factor TWEAK (TNFSF12) can induce a UC-like inflammatory profile in colonic fibroblasts in vitro ,...

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Literature Corpus work
a2c77575-330c-54f7-aecd-a71781236f10
DOI
10.1101/2025.09.23.678006
Open publication

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TWEAK is increased in ulcerative colitis and contributes to fibroblast-mediated monocyte activation via heterologous non-canonical NF-kB/STAT3 signallingDOI 10.1101/2025.09.23.678006
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