Intravenous immunoglobulin inhibits BAFF production in chronic inflammatory demyelinating polyneuropathy - a new mechanism of action?
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.
Dept. of Neurology, Justus-Liebig-University, Am Steg 16, D-35392Giessen, Germany.
Sandra
S
Bick
Marlene
M
Tschernatsch
Anne
A
Karg
Verena
V
Fuehlhuber
Tina E
TE
Trenczek
Kathrin
K
Faltermeier
Holger
H
Hackstein
Manfred
M
Kaps
Franz
F
Blaes
D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D053264:B-Cell Activating Factor / Q000097:blood* / Q000235:genetics; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000008:administration & dosage* / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D020277:Polyradiculoneuropathy, Chronic Inflammatory Demyelinating / Q000097:blood / Q000276:immunology / Q000628:therapy; D012333:RNA, Messenger / Q000378:metabolism; D013997:Time Factors
D053264:B-Cell Activating Factor; D016756:Immunoglobulins, Intravenous; D012333:RNA, Messenger; C505719:TNFSF13B protein, human