Introduction: Inflammatory bowel diseases (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), present ongoing challenges despite advances in pathophysiological understanding and therapeutic options. Current therapies often fail to achieve sustained remission, necessitating exploration of novel treatment targets.
Areas covered: This review explores the role of Tumor Necrosis Factor-like cytokine 1A (TL1A) and its receptor DR3 in IBD pathogenesis, detailing their involvement in mucosal homeostasis and immune modulation. Recent studies on TL1A inhibitors highlight their potential in mitigating inflammation and fibrosis in IBD.
Expert opinion: TL1A inhibition emerges as a promising therapeutic strategy, supported by encouraging outcomes in clinical trials for moderate to severe IBD. Future research may elucidate TL1A's broader impact on immunity, epithelial integrity and fibrosis, offering new avenues for therapeutic intervention and biomarker discovery. Ongoing phase 3 trials are pivotal in assessing TL1A inhibitors as effective and safe treatments for IBD. Additionally, exploration of TL1A's role in fibrosis-associated complications and its potential as a biomarker for treatment response holds promise for personalized medicine approaches. Consideration of TL1A inhibition in concurrent immune-mediated inflammatory diseases suggests broader therapeutic implications beyond gastrointestinal manifestations of IBD.
Keywords: Crohn’s disease; DR3 receptor; TL1A inhibitor; fibrosis; inflammatory bowel disease; ulcerative colitis.