Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3064298 | Journal of Neuroimmunology | 2013 | 7 Pages |
Abstract
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, Fcγ-receptor independent, mechanism of action for IVIg.
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Authors
Sandra Bick, Marlene Tschernatsch, Anne Karg, Verena Fuehlhuber, Tina E. Trenczek, Kathrin Faltermeier, Holger Hackstein, Manfred Kaps, Franz Blaes,