THE ROLE OF CHEMOKINES IN GUILLAIN-BARRE SYNDROME

被引:30
作者
Chiang, Sharon [1 ]
Ubogu, Eroboghene E. [2 ]
机构
[1] Rice Univ, Dept Stat, Houston, TX 77251 USA
[2] Baylor Coll Med, Dept Neurol, Neuromuscular Immunopathol Res Lab, Houston, TX 77030 USA
基金
美国国家卫生研究院;
关键词
chemokine; chemokine receptor; experimental autoimmune neuritis; Guillain-Barre syndrome; therapy; EXPERIMENTAL AUTOIMMUNE NEURITIS; ALPHA THERAPY; EXPRESSION; RECEPTORS; NEUROPATHIES; MODEL; IDENTIFICATION; CYTOKINES; CELLS;
D O I
10.1002/mus.23829
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction: Chemokines and their receptors are important mediators of inflammation. Guillain-Barre syndrome (GBS) is the most common cause of acute paralysis worldwide. Despite current treatments, outcomes are suboptimal. Specific chemokine receptor antagonists have the potential to be efficacious against pathogenic leukocyte trafficking in GBS. Methods: A 36-year literature review was performed to summarize available data on chemokine expression in GBS and its representative animal model, experimental autoimmune neuritis (EAN). Results: Although there were a few observational human and animal studies demonstrating chemokine ligand/receptor expression in GBS and EAN, in vitro and in vivo functional studies using gene knockouts, neutralizing antibodies, or small molecular antagonists were limited. CCL2-CCR2, CCL5-CCR5, and CXCL10-CXCR3 have been most strongly implicated in EAN and GBS pathogenesis, providing targets for molecular blockade. Conclusions: Preclinical human in vitro and in vivo EAN studies are needed to evaluate the potential efficacy of chemokine signaling inhibition in GBS. Muscle Nerve48: 320-330, 2013
引用
收藏
页码:320 / 330
页数:11
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