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Cited by 521

The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.

Abnormal B‐cell cytokine responses a trigger of T‐cell–mediated disease in MS?

Bar‐Or, Amit, Fawaz, Lama, Fan, Boli, Darlington, Peter J., Rieger, Aja, Ghorayeb, Christine, Calabresi, Peter A., Waubant, Emmanuelle, Hauser, Stephen L., Zhang, Jiameng, Smith, Craig H.·2010·Annals of Neurology
DOI 10.1002/ana.21939
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Abstract

Objective: To study antibody‐independent contributions of B cells to inflammatory disease activity, and the immune consequences of B‐cell depletion with rituximab, in patients with multiple sclerosis (MS). Methods: B‐Cell effector‐cytokine responses were compared between MS patients and matched controls using a 3‐signal model of activation. The effects of B‐cell depletion on Th1/Th17 CD4 and CD8 T‐cell responses in MS patients were assessed both ex vivo and in vivo, together with pharmacokinetic/pharmacodynamic studies as part of 2 rituximab clinical trials in relapsing–remitting MS. Results: B Cells of MS patients exhibited aberrant proinflammatory cytokine responses, including increased lymphotoxin (LT):interleukin‐10 ratios and exaggerated LT and tumor necrosis factor (TNF)‐α secretion, when activated in the context of the pathogen‐associated TLR9‐ligand CpG‐DNA, or the Th1 cytokine interferon‐γ, respectively. B‐Cell depletion, both ex vivo and in vivo, resulted in significantly diminished proinflammatory (Th1 and Th17) responses of both CD4 and CD8 T cells. Soluble products from activated B cells of untreated MS patients reconstituted the diminished T‐cell responses observed following in vivo B‐cell depletion in the same patients, and this effect appeared to be largely mediated by B‐cell LT and TNFα. Interpretation: We propose that episodic triggering of abnormal B‐cell cytokine responses mediates ‘bystander activation’ of disease‐relevant proinflammatory T cells, resulting in new relapsing MS disease activity. Our findings point to a plausible mechanism for the long‐recognized association between infections and new MS relapses, and provide novel insights into B‐cell roles in both health and disease, and into mechanisms contributing to therapeutic effects of B‐cell depletion in human autoimmune diseases, including MS. ANN NEUROL 2010;67:452–461

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Metadata

Authors
Bar‐Or, A., Fawaz, L., Fan, B., Darlington, P. J., Rieger, A., Ghorayeb, C., Calabresi, P. A., Waubant, E., Hauser, S. L., Zhang, J., & Smith, C. H.
Venue
Annals of Neurology
Publisher
Wiley
Published
2010-04
Volume
67
Issue
4
Pages
452-461
ISSN
  • 0364-5134 (ISSN-L)
  • 1531-8249
DOI
10.1002/ana.21939
OpenAlex
W1981621288
Cited by
521
References
42
FWCI
12.62
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Abnormal B‐cell cytokine responses a trigger of T‐cell–mediated disease in MS? https://app.cochat.ai/papers/10.1002/ana.21939
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Bar‐Or, A., Fawaz, L., Fan, B., Darlington, P. J., Rieger, A., Ghorayeb, C., Calabresi, P. A., Waubant, E., Hauser, S. L., Zhang, J., & Smith, C. H. (2010). Abnormal B‐cell cytokine responses a trigger of T‐cell–mediated disease in MS? Annals of Neurology. https://doi.org/10.1002/ana.21939

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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