TL1A: A Key Emerging Pathway in Inflflammatory

About Webinar

Inflammatory bowel disease (IBD) remains a complex and heterogeneous disorder in which chronic intestinal inflammation results from a multifactorial interplay of genetic susceptibility, environmental factors, and immune dysregulation. Despite major therapeutic progress, a considerable proportion of patients continue to experience suboptimal response, loss of efficacy, or disease progression, underscoring the need for innovative and mechanistically targeted treatment approaches. Among the pathways currently under investigation, TL1A has emerged as a key mediator of mucosal inflammation and fibrosis. Acting through its receptor DR3, TL1A amplifies T-cell activation, promotes Th1/ Th17 polarization, and enhances pro-inflammatory cytokine cascades. Preclinical and early clinical data suggest that selective blockade of the TL1A/DR3 axis may attenuate inflammation, reduce fibrotic remodeling, and offer a novel therapeutic strategy across both ulcerative colitis and Crohn’s disease.