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<p>Tumor necrosis factor-like cytokine 1&#xa0;A (TL1A), encoded by the TNFSF15 gene, is expressed on multiple cells, including endothelial cells and dendritic cells, and in a soluble form in serum. Due to its central role in regulating immune response, TL1A has been implicated in the pathogenesis of several autoimmune inflammatory diseases such as inflammatory bowel disease (IBD), psoriasis and rheumatoid arthritis (RA). Mechanistically, TL1A exerts proinflammatory effects through binding of death receptor 3 (DR3) to activate downstream signalling cascades that drive inflammation and apoptosis. Tulisokibart, a novel humanized anti-TL1A monoclonal antibody, has garnered significant attention following phase 2 clinical trials demonstrating robust efficacy in IBD. Additional anti-TL1A drugs, afimkibart and duvakitug, are progressing rapidly through clinical development pipeline across multiple indications, underscoring the broad therapeutic potential of TL1A blockade. This review delineates the pathomechanistic basis of anti-TL1A therapies and explores emerging clinical applications. Moreover, to facilitate precision medicine approaches and optimize therapeutic outcomes among different population subgroups, we analyse the potential impact of genetic polymorphisms on individual responses to TL1A-targeted therapy. Taken together, anti-TL1A therapies hold considerable promise for modulating adaptive and immune pathways and represent an innovative strategy for treating complex inflammatory diseases.</p>

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Therapeutic Potential of Tulisokibart and Anti-TL1A Therapy in Inflammatory Disorders: Current Insights and Future Directions

  • 期刊论文

  • 发表日期：

    2026年3月28日

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  • Juling Sia,
  • Bernett Lee,
  • Hazel H. Oon

摘要

Tumor necrosis factor-like cytokine 1 A (TL1A), encoded by the TNFSF15 gene, is expressed on multiple cells, including endothelial cells and dendritic cells, and in a soluble form in serum. Due to its central role in regulating immune response, TL1A has been implicated in the pathogenesis of several autoimmune inflammatory diseases such as inflammatory bowel disease (IBD), psoriasis and rheumatoid arthritis (RA). Mechanistically, TL1A exerts proinflammatory effects through binding of death receptor 3 (DR3) to activate downstream signalling cascades that drive inflammation and apoptosis. Tulisokibart, a novel humanized anti-TL1A monoclonal antibody, has garnered significant attention following phase 2 clinical trials demonstrating robust efficacy in IBD. Additional anti-TL1A drugs, afimkibart and duvakitug, are progressing rapidly through clinical development pipeline across multiple indications, underscoring the broad therapeutic potential of TL1A blockade. This review delineates the pathomechanistic basis of anti-TL1A therapies and explores emerging clinical applications. Moreover, to facilitate precision medicine approaches and optimize therapeutic outcomes among different population subgroups, we analyse the potential impact of genetic polymorphisms on individual responses to TL1A-targeted therapy. Taken together, anti-TL1A therapies hold considerable promise for modulating adaptive and immune pathways and represent an innovative strategy for treating complex inflammatory diseases.