Intravenous immunoglobulin inhibits BAFF production in chronic inflammatory demyelinating polyneuropathy - A new mechanism of action?

被引：28

作者：

Bick, Sandra ^{[1
]}

Tschernatsch, Marlene ^{[1
]}

Karg, Anne ^{[1
]}

Fuehlhuber, Verena ^{[1
]}

Trenczek, Tina E. ^{[2
]}

Faltermeier, Kathrin ^{[1
]}

Hackstein, Holger ^{[3
]}

Kaps, Manfred ^{[1
]}

Blaes, Franz ^{[1
,4
]}

机构：

[1] Univ Giessen, Dept Neurol, D-35392 Giessen, Germany

[2] Univ Giessen, Inst Gen & Special Zool, D-35390 Giessen, Germany

[3] Univ Giessen, Dept Clin Immunol & Transfus Med, D-35385 Giessen, Germany

[4] Gummersbach Hosp, Dept Neurol, D-51643 Gummersbach, Germany

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2013年 / 256卷 / 1-2期

关键词：

B-cell activating factor; CIDP; IVIg; Monocytes; NF-KAPPA-B; ACTIVATING FACTOR BAFF; NECROSIS-FACTOR FAMILY; LYMPHOCYTE STIMULATOR; IVIG PREPARATIONS; POLYRADICULONEUROPATHY; EXPRESSION; CELLS; DERMATOMYOSITIS; OVEREXPRESSION;

D O I：

10.1016/j.jneuroim.2013.01.001

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Chronic-inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated disease treated with intravenous immunoglobulin (IVIg). The underlying mechanism of action remains incompletely understood. The B-cell activating factor BAFF contributes to B-cell homeostasis and (auto-)antibody production. BAFF was recently identified as one key molecule in the development of autoimmune diseases. Herein, we demonstrate that BAFF serum levels are elevated in CIDP patients. IVIg treatment resulted in a significant decrease of BAFF serum level. In vitro, IVIg inhibited BAFF in monocytes. Consequently, we identified BAFF as a new target for IVIg in CIDP treatment and provide a new, Fc gamma-receptor independent, mechanism of action for IVIg. (C) 2013 Elsevier B.V. All rights reserved.

引用

页码：84 / 90

页数：7

共 48 条

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