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@ARTICLE{Ritter:201384,
      author       = {Ritter, Christian and Förster, Dominik and Albrecht,
                      Philipp and Hartung, Hans-Peter and Kieseier, Bernd C. and
                      Lehmann, Helmar C.},
      title        = {{IVIG} regulates {BAFF} expression in patients with chronic
                      inflammatory demyelinating polyneuropathy ({CIDP})},
      journal      = {Journal of neuroimmunology},
      volume       = {274},
      number       = {1-2},
      issn         = {0165-5728},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2015-03679},
      pages        = {225 - 229},
      year         = {2014},
      abstract     = {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.},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {333 - Pathophysiological Mechanisms of Neurological and
                      Psychiatric Diseases (POF2-333)},
      pid          = {G:(DE-HGF)POF2-333},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000342871600030},
      pubmed       = {pmid:25002077},
      doi          = {10.1016/j.jneuroim.2014.06.007},
      url          = {https://juser.fz-juelich.de/record/201384},
}