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- W4327855563 abstract "Introduction Patients suffering from inflammatory bowel diseases (IBDs) are primarily treated with existing immune modulators. However, patients not responding to therapy still exist. Recent studies have revealed neutrophil-related-molecular signatures as part of non-effective treatment among therapy-refractory subgroups within ulcerative colitis (UC) patients [1]. Previously, we reported that mucosal healing is highly influenced by effector processes of neutrophil granulocytes [2] [4] [5] [6]. The effector function of neutrophils is mediated by inflammatory cytokines [3]. Proinflammatory cytokines like IL36α and IL36γ have been reported to induce proliferation and production of antimicrobial peptides by IECs and mediate the chemotaxis of neutrophils towards the ulceration [4]. Our new data indicates that IL36R ligands shape wound-associated-epithelial (WAE) cells and neutrophil cell activities as evidenced in vivo and in vitro. We aim to understand the role of IL36 mediated crosstalk between WAE cells and granulocytes in order to evaluate new treatment options for therapy-refractory IBD patients." @default.
- W4327855563 created "2023-03-20" @default.
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- W4327855563 date "2023-03-01" @default.
- W4327855563 modified "2023-09-23" @default.
- W4327855563 title "IL36R signaling in intestinal epithelial cells and neutrophils enhances intestinal wound healing" @default.
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- W4327855563 doi "https://doi.org/10.1055/s-0043-1764068" @default.
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