JAK–STAT pathway targeting for the treatment of inflammatory bowel disease

医学 炎症性肠病 斯达 JAK-STAT信号通路 炎症性肠病 克罗恩病 疾病 癌症研究 免疫学 车站3 内科学 胃肠病学 信号转导 生物 受体 遗传学 酪氨酸激酶
作者
Azucena Salas,Cristian Hernández-Rocha,Marjolijn Duijvestein,William A. Faubion,Dermot McGovern,Séverine Vermeire,Stefania Vetrano,Niels Vande Casteele
出处
期刊:Nature Reviews Gastroenterology & Hepatology [Nature Portfolio]
卷期号:17 (6): 323-337 被引量:483
标识
DOI:10.1038/s41575-020-0273-0
摘要

Cytokines are involved in intestinal homeostasis and pathological processes associated with inflammatory bowel disease (IBD). The biological effects of cytokines, including several involved in the pathology of Crohn’s disease and ulcerative colitis, occur as a result of receptor-mediated signalling through the Janus kinase (JAK) and signal transducer and activator of transcription (STAT) DNA-binding families of proteins. Although therapies targeting cytokines have revolutionized IBD therapy, they have historically targeted individual cytokines, and an unmet medical need exists for patients who do not respond to or lose response to these treatments. Several small-molecule inhibitors of JAKs that have the potential to affect multiple pro-inflammatory cytokine-dependent pathways are in clinical development for the treatment of IBD, with one agent, tofacitinib, already approved for ulcerative colitis and several other agents with demonstrated efficacy in early phase trials. This Review describes the current understanding of JAK–STAT signalling in intestinal homeostasis and disease and the rationale for targeting this pathway as a treatment for IBD. The available evidence for the efficacy, safety and pharmacokinetics of JAK inhibitors in IBD as well as the potential approaches to optimize treatment with these agents, such as localized delivery or combination therapy, are also discussed. The biological effects of cytokines in intestinal homeostasis and disease occur as a result of JAK–STAT signalling. This Review describes the current understanding of JAK–STAT signalling in intestinal homeostasis and inflammatory bowel disease as well as the rationale for therapeutically targeting this pathway.
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