Alimentary pharmacology & therapeutics · 2026
Review Article: TL1A Inhibitors in IBD - Mechanistic Rationale and Clinical Evidence.
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Goyal Manjeet Kumar, Srivastava Harsh, Sehgal Tanisha, Bishu Shrinivas, Sharma Vishal, Sebastian Shaji
Аннотация
BACKGROUND: Tumour necrosis factor-like ligand 1A (TL1A) and its receptor DR3 form a pivotal signalling dyad linking immune activation, epithelial barrier dysfunction and fibrogenesis in inflammatory bowel diseases. (IBD).
AIMS: This narrative review summarizes the molecular biology of the TL1A-DR3 axis, its roles in intestinal inflammation, fibrosis, and extraintestinal manifestations, and the emerging therapeutic landscape of TL1A inhibition in IBD.
METHODS: Narrative synthesis of preclinical, translational, and clinical literature on TL1A/DR3 in Crohn's disease and ulcerative colitis.
RESULTS: TL1A overexpression drives Crohn's-like ileitis, barrier disruption, and fibrosis in models; blockade attenuates both inflammation and remodelling. TL1A inhibitors show clinical/endoscopic remission in early-phase moderate-severe IBD trials (e.g., tulisokibart, duvakitug), with phase 3 programs ongoing.
CONCLUSION: TL1A-DR3 integrates mucosal immunity with stromal injury, positioning inhibitors as a novel class to overcome IBD therapeutic ceilings by targeting the inflammation-fibrosis continuum.
AIMS: This narrative review summarizes the molecular biology of the TL1A-DR3 axis, its roles in intestinal inflammation, fibrosis, and extraintestinal manifestations, and the emerging therapeutic landscape of TL1A inhibition in IBD.
METHODS: Narrative synthesis of preclinical, translational, and clinical literature on TL1A/DR3 in Crohn's disease and ulcerative colitis.
RESULTS: TL1A overexpression drives Crohn's-like ileitis, barrier disruption, and fibrosis in models; blockade attenuates both inflammation and remodelling. TL1A inhibitors show clinical/endoscopic remission in early-phase moderate-severe IBD trials (e.g., tulisokibart, duvakitug), with phase 3 programs ongoing.
CONCLUSION: TL1A-DR3 integrates mucosal immunity with stromal injury, positioning inhibitors as a novel class to overcome IBD therapeutic ceilings by targeting the inflammation-fibrosis continuum.