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| 001 | 201384 | ||
| 005 | 20210129215736.0 | ||
| 024 | 7 | _ | |a 10.1016/j.jneuroim.2014.06.007 |2 doi |
| 024 | 7 | _ | |a 0165-5728 |2 ISSN |
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| 100 | 1 | _ | |a Ritter, Christian |0 P:(DE-Juel1)156467 |b 0 |
| 245 | _ | _ | |a IVIG regulates BAFF expression in patients with chronic inflammatory demyelinating polyneuropathy (CIDP) |
| 260 | _ | _ | |a Amsterdam [u.a.] |c 2014 |b Elsevier Science |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1435123409_21685 |2 PUB:(DE-HGF) |
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| 520 | _ | _ | |a Recent studies indicate that the cytokine B-cell activating factor (BAFF) is involved in the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP). Intravenous immunoglobulin (IVIg) is standard treatment for CIDP and is known to rapidly modulate increased serum levels of pro-inflammatory cytokines. We evaluated the expression profile of BAFF and its corresponding BAFF-receptor in samples from CIDP patients, focusing on rapid changes before and after IVIg treatment. In CIDP patients BAFF serum concentrations were elevated compared to controls. Treatment with high-dose IVIg restored those elevated BAFF serum levels. Whereas treatment with IVIg did not affect BAFF production in monocytes, antibodies against BAFF could be detected in IVIg preparations, which may explain the short-term decrease of BAFF levels after IVIg treatment. Our data suggest that BAFF plays an important role in the pathogenesis of CIDP and may serve as marker for IVIg treatment response. |
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| 700 | 1 | _ | |a Förster, Dominik |0 P:(DE-HGF)0 |b 1 |
| 700 | 1 | _ | |a Albrecht, Philipp |0 P:(DE-HGF)0 |b 2 |
| 700 | 1 | _ | |a Hartung, Hans-Peter |0 P:(DE-HGF)0 |b 3 |
| 700 | 1 | _ | |a Kieseier, Bernd C. |0 P:(DE-HGF)0 |b 4 |
| 700 | 1 | _ | |a Lehmann, Helmar C. |0 P:(DE-HGF)0 |b 5 |e Corresponding Author |
| 773 | _ | _ | |a 10.1016/j.jneuroim.2014.06.007 |g Vol. 274, no. 1-2, p. 225 - 229 |0 PERI:(DE-600)1500497-1 |n 1-2 |p 225 - 229 |t Journal of neuroimmunology |v 274 |y 2014 |x 0165-5728 |
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