Interfering with leukocyte trafficking in Crohn's disease

被引：21

作者：

Biswas, Sujata ^{[1
]}

Bryant, Robert V. ^{[2
]}

Travis, Simon ^{[1
]}

机构：

[1] Oxford Univ Hosp NHS Fdn Trust, John Radcliffe Hosp, Translat Gastroenterol Unit, NIHR Oxford Biomed Res Ctr, Oxford OX3 9DU, England

[2] Queen Elizabeth Hosp, Dept Gastroenterol, IBD Serv, Adelaide, SA 5011, Australia

来源：

BEST PRACTICE & RESEARCH CLINICAL GASTROENTEROLOGY | 2019年 / 38-39卷

关键词：

Crohn's; Leukocyte trafficking; Integrins; Chemokines; INTERCELLULAR-ADHESION MOLECULE-1; INFLAMMATORY-BOWEL-DISEASE; INDUCTION THERAPY; ULCERATIVE-COLITIS; CELL-ADHESION; MAINTENANCE THERAPY; DOUBLE-BLIND; VEDOLIZUMAB; PLACEBO; SAFETY;

D O I：

10.1016/j.bpg.2019.05.004

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

100201 [内科学];

摘要：

The discovery of gut-specific leukocytes and the ability to modulate their function has been a ground-breaking development in the treatment of inflammatory bowel disease. Drugs target the interaction between lymphocytes and endothelial cells via integrins and their ligand cellular adhesion molecules. Safety, efficacy and sustainability of effect are key to this drug class, notwithstanding the association of natalizumab with fatal polyoma virus infection. Vedolizumab (2014) now licensed for the treatment of Crohn's disease around the world provides gut-specific immunosuppression. Targets for modulators of leukocyte trafficking include (examples in brackets) ICAM-1 (alicaforsen, efalizumab); MAdCAM-1 (PF-00547 659); alpha 4 and related receptors (abrilumab, etrolizumab, natalizumab, vedolizumab); chemokine receptor CCR9 (vercirnon); and sphingosine 1-phosphate receptors (etrasimod, fingolimod, ozanimod). Oral and subcutaneous therapies are in development. The safety, efficacy and practice points of licensed drugs are discussed, in addition to initial results from therapeutic trials. Crown Copyright (C) 2019 Published by Elsevier Ltd. All rights reserved.

引用

页数：8

共 54 条

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Intercellular adhesion molecule-1 (ICAM-1) deficiency protects mice against severe forms of experimentally induced colitis [J].