Chemokines as Novel Therapeutic Targets for Inflammatory Bowel Disease

Chemokines as Novel Therapeutic Targets for Inflammatory Bowel Disease
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DOI:
10.1111/j.1749-6632.2009.04738.x
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发表时间:
2009-01-01
期刊:
CONTEMPORARY CHALLENGES IN AUTOIMMUNITY
影响因子:
--
通讯作者:
Imai, Toshio
Imai, Toshio
中科院分区:
其他
文献类型:
--
作者:
Nishimura, Miyuki;Kuboi, Yoshikazu;Imai, Toshio

文献摘要

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炎症性肠病(IBD)如克罗恩病(CD)和溃疡性结肠炎(UC)是以与胃肠道的自毁性炎症相关的复发和缓解的慢性临床过程为特征的疾病。在UC和CD中,白细胞浸润到肠中是疾病发展和进展中的基本事件,其中趋化因子及其受体协调白细胞的组织特异性和细胞类型选择性运输。在这篇综述中,我们将讨论趋化因子及其受体的稳态和炎症作用及其作为人类IBD治疗干预的分子靶点的潜力和前景,重点关注最近确定的CX 3CL 1-CX 3CR 1轴的作用,以及CCL 20-CCR 6,CCL 25-CCR 9和CXCL 10-CXCR 3途径。
The inflammatory bowel diseases (IBD) such as Crohn's disease (CD) and ulcerative colitis (UC) are illness characterized by a chronic clinical course of relapse and remission associated with self-destructive inflammation of the gastrointestinal tract. In both UC and CD, leukocyte infiltration into the intestine is fundamental event in disease development and progression where the chemokines and their receptors are orchestrating the tissue-specific and the cell type-selective trafficking of leukocytes. In this review, we will discuss the homeostatic and inflammatory roles of the chemokines and their receptors with their potentials and promise as molecular targets for therapeutic interventions in human IBD, focusing on the recently identified role of the CX3CL1-CX3CR1 axis, as well as the CCL20-CCR6, CCL25-CCR9, and CXCL10-CXCR3 pathways.