发病机制
炎症性肠病
细胞因子
医学
疾病
胃肠道
溃疡性结肠炎
克罗恩病
免疫学
内科学
肿瘤坏死因子α
作者
Federica Furfaro,Ludovico Alfarone,Daniela Gilardi,Carmen Correale,Mariangela Allocca,Gionata Fiorino,Silvio Danese,Alessandra Zilli,Eirini Zacharopoulou,Laura Loy,Giulia Roda,Silvio Danese
出处
期刊:Current Drug Targets
[Bentham Science]
日期:2021-01-26
卷期号:22 (7): 760-769
被引量:18
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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