@article{GernertSchmalzingTonyetal.2022,
  author    = {Gernert, Michael and Schmalzing, Marc and Tony, Hans-Peter and Strunz, Patrick-Pascal and Schwaneck, Eva Christina and Fr{\"o}hlich, Matthias},
  title     = {Calprotectin (S100A8/S100A9) detects inflammatory activity in rheumatoid arthritis patients receiving tocilizumab therapy},
  series = {Arthritis Research \& Therapy},
  volume    = {24},
  journal   = {Arthritis Research \& Therapy},
  number    = {1},
  doi       = {10.1186/s13075-022-02887-7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-300523},
  year      = {2022},
  abstract  = {Background Assessing serological inflammation is difficult in tocilizumab (TCZ)-treated rheumatoid arthritis (RA) patients, as standard inflammation parameters, like erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), are influenced by interleukin-6-receptor inhibition. Calprotectin in the serum, also named S100A8/S100A9, might be a more useful inflammation parameter in TCZ-treated patients. Methods Sixty-nine RA patients taking TCZ were included. Serum-calprotectin levels were assessed, as well as ESR, CRP, need for a change in disease-modifying anti-rheumatic drugs due to RA activity (= active RA), and the RA clinical disease activity score (CDAI). Forty-five RA patients taking tumor-necrosis factor-inhibitors (TNFi) were investigated for the same parameters. Results TCZ-treated patients with active RA had higher calprotectin values than not active RA patients (4155.5 [inter quartile range 1865.3-6068.3] vs 1040.0 [676.0-1638.0] ng/ml, P < 0.001). A calprotectin cut-off value of 1916.5 ng/ml resulted in a sensitivity and specificity of 80.0 \%, respectively, for the detection of RA disease activity. Calprotectin values correlated with CDAI-scores (r = 0.228; P = 0.011). ESR and CRP were less suitable to detect RA activity in TCZ-treated patients. Also TNFi-treated patients with active RA had higher calprotectin values compared to not active RA (5422.0 [3749.0-8150.8] vs 1845.0 [832.0-2569.0] ng/ml, P < 0.001). The calprotectin value with the best sensitivity and specificity for detecting RA activity was 3690.5 ng/ml among TNFi-treated patients. Conclusion Calprotectin in the serum can be a useful inflammation parameter despite TCZ-treatment.},
  language  = {en}
}
@article{TraubHusseiniWeber2021,
  author    = {Traub, Jan and Husseini, Leila and Weber, Martin S.},
  title     = {B cells and antibodies as targets of therapeutic intervention in neuromyelitis optica spectrum disorders},
  series = {Pharmaceuticals},
  volume    = {14},
  journal   = {Pharmaceuticals},
  number    = {1},
  issn      = {1424-8247},
  doi       = {10.3390/ph14010037},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-222957},
  year      = {2021},
  abstract  = {The first description of neuromyelitis optica by Eug{\`e}ne Devic and Fernand Gault dates back to the 19th century, but only the discovery of aquaporin-4 autoantibodies in a major subset of affected patients in 2004 led to a fundamentally revised disease concept: Neuromyelits optica spectrum disorders (NMOSD) are now considered autoantibody-mediated autoimmune diseases, bringing the pivotal pathogenetic role of B cells and plasma cells into focus. Not long ago, there was no approved medication for this deleterious disease and off-label therapies were the only treatment options for affected patients. Within the last years, there has been a tremendous development of novel therapies with diverse treatment strategies: immunosuppression, B cell depletion, complement factor antagonism and interleukin-6 receptor blockage were shown to be effective and promising therapeutic interventions. This has led to the long-expected official approval of eculizumab in 2019 and inebilizumab in 2020. In this article, we review current pathogenetic concepts in NMOSD with a focus on the role of B cells and autoantibodies as major contributors to the propagation of these diseases. Lastly, by highlighting promising experimental and future treatment options, we aim to round up the current state of knowledge on the therapeutic arsenal in NMOSD.},
  language  = {en}
}