炎症性肠病
溃疡性结肠炎
发病机制
免疫系统
受体
调节器
诱饵
免疫学
信号转导
医学
结肠炎
炎症
细胞因子
配体(生物化学)
下调和上调
疾病
促炎细胞因子
细胞生物学
获得性免疫系统
克罗恩病
化学
计算生物学
炎症性肠病
先天免疫系统
免疫
肿瘤坏死因子α
癌症研究
生物
生物信息学
作者
Cameron L Noland,Marcelo Murai,Paulo Zaragoza,Ben Bell,Sultan Yilmaz,Shruti Nayak,Esme Alarcon,Michael Eddins,Todd Mayhood,Yunpeng Zhou,Burt Barnett,Haihong Zhou,Johan Fransson
摘要
TNF-like ligand 1A (TL1A) is a pro-inflammatory cytokine that is a critical regulator of mucosal immunity and has been implicated in the pathogenesis of Inflammatory Bowel Disease (IBD). TL1A is expressed on antigen-presenting cells and binds to its functional receptor, death- domain receptor 3 (DR3), on T cells to activate pro-inflammatory pathways that are integral to the adaptive immune response. In contrast, binding to soluble decoy receptor 3 (DcR3) prevents pathway signaling through direct competition with DR3. TL1A is upregulated in inflamed IBD tissue, and blocking TL1A has shown promise in Ph2 ulcerative colitis and Crohn’s disease studies. However, the structural understanding of the TL1A- DR3 interaction is incomplete, as only the structure of TL1A bound to DcR3 has been elucidated. To gain insights into the molecular nature of the TL1A-DR3 interaction, we solved the structure of this complex to 2.8 Å resolution using cryo-electron microscopy. The structure reveals that DR3 engages TL1A in a manner akin to DcR3, but with several distinct features. Overall, this work deepens our understanding of TL1A-DR3 interactions and lends valuable insights to the development of TL1A inhibitors as a potential treatment for IBD.
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