发病机制
炎症性肠病
细胞因子
医学
疾病
炎症性肠病
溃疡性结肠炎
促炎细胞因子
坏死
结肠炎
免疫
调节器
英夫利昔单抗
克罗恩病
免疫学
受体
免疫系统
内科学
肿瘤坏死因子α
炎症
肿瘤坏死因子α
生物药物
炎症反应
作者
Federica Furfaro,Ludovico Alfarone,Daniela Gilardi,Carmen Correale,Mariangela Allocca,Gionata Fiorino,Marjorie Argollo,Alessandra Zilli,Eirini Zacharopoulou,Laura Loy,Giulia Roda,Silvio Danese
标识
DOI:10.2174/1389450122999210120205607
摘要
Inflammatory bowel diseases (IBD), including ulcerative colitis (UC) and Crohn’s disease (CD), are chronic inflammatory diseases of the gastrointestinal tract. In the last few years, the development of biological agents targeting cytokines and receptors involved in IBD pathogenesis has led to better outcomes and has improved the course of the disease. Despite their effectiveness, drugs such as tumor necrosis factor (TNF) inhibitors, anti-Interleukin-12/23 and anti-integrins, do not induce a response in about one-third of patients, and 40% of patients lose response over time. Therefore, more efficient therapies are required. Recent studies showed that TL1A (Tumor necrosis factor-like cytokine 1A) acts as a regulator of mucosal immunity and participates in immunological pathways involved in the IBD pathogenesis. In this review article, we analyze the role of TL1A as a new potential target therapy in IBD patients.
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