Journalartikel

Jahr der Veröffentlichung: 2013

Seiten: 84-90

Zeitschrift: Journal of Neuroimmunology

Bandnummer: 256

Heftnummer: 1-2

ISSN: 0165-5728

DOI Link: https://doi.org/10.1016/j.jneuroim.2013.01.001

Verlag: Elsevier

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.

Harvard-Zitierstil: Bick, S., Tschernatsch, M., Karg, A., Fuehlhuber, V., Trenczek, T., Faltermeier, K., et al. (2013) Intravenous immunoglobulin inhibits BAFF production in chronic inflammatory demyelinating polyneuropathy : a new mechanism of action?, Journal of Neuroimmunology, 256(1-2), pp. 84-90. https://doi.org/10.1016/j.jneuroim.2013.01.001

APA-Zitierstil: Bick, S., Tschernatsch, M., Karg, A., Fuehlhuber, V., Trenczek, T., Faltermeier, K., Hackstein, H., Kaps, M., & Blaes, F. (2013). Intravenous immunoglobulin inhibits BAFF production in chronic inflammatory demyelinating polyneuropathy : a new mechanism of action?. Journal of Neuroimmunology. 256(1-2), 84-90. https://doi.org/10.1016/j.jneuroim.2013.01.001