Therapeutic leukocytapheresis for inflammatory bowel disease

被引:68
|
作者
Saniabadi, Abbi R. [1 ]
Hanai, Hiroyuki [2 ]
Fukunaga, Ken [3 ]
Sawada, Koji [4 ]
Shima, Chikako [1 ]
Bjarnason, Ingvar [5 ]
Lofberg, Robert [6 ]
机构
[1] JIMRO Labs, Takasaki, Gunma 3700021, Japan
[2] Hamamatsu S Hosp, Hamamatsu, Shizuoka 4300846, Japan
[3] Hyogo Coll Med, Nishinomiya, Hyogo 663, Japan
[4] Fujimoto Hosp Med, Osaka 5830857, Japan
[5] GKT Med Sch, London, England
[6] Karolinska Inst, Stockholm, Sweden
关键词
inflammatory bowel disease; granulocytes; proinfammatory CD14(+)CD16(+) monocytes; selective leukocytapheresis; regulatory CD4(+)CD25(+)Foxp3 T cells; Adacolumn;
D O I
10.1016/j.transci.2007.08.003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The inference that granulocytes and monocytes/macrophages (GM) are part of the immunopathogenesis of inflammatory bowel disease (IBD) and hence should be targets of therapy stems from observations of elevated, and activated GM in patients with IBD. The Adacolumn can selectively deplete GM by adsorption (GMA) and in patients with IBD, GMA has been associated with significant clinical efficacy together with sustained suppression of inflammatory cytokine profiles. Additionally, GMA depleted proinflammatory CD 14(+)CD 16(+) monocytes and was followed by an increase in CD4(+) T lymphocytes including the regulatory CD4(+)CD25(high+)Foxp3 phenotype. Hence, GMA could be a non-pharmacologic therapy for IBD with potential to spare steroids and other unsafe pharmacologic preparations. (C) 2007 Published by Elsevier Ltd.
引用
收藏
页码:191 / 200
页数:10
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