Role of B Cells in Multiple Sclerosis and Related Disorders
Publikation: Bidrag til tidsskrift › Review › Forskning › fagfællebedømt
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The success of clinical trials of selective B-cell depletion in patients with relapsing multiple sclerosis (MS) and primary progressive MS has led to a conceptual shift in the understanding of MS pathogenesis, away from the classical model in which T cells were the sole central actors and toward a more complex paradigm with B cells having an essential role in both the inflammatory and neurodegenerative components of the disease process. The role of B cells in MS was selected as the topic of the 27th Annual Meeting of the European Charcot Foundation. Results of the meeting are presented in this concise review, which recaps current concepts underlying the biology and therapeutic rationale behind B-cell–directed therapeutics in MS, and proposes strategies to optimize the use of existing anti–B-cell treatments and provide future directions for research in this area. ANN NEUROL 2021;89:13–23.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Annals of Neurology |
| Vol/bind | 89 |
| Udgave nummer | 1 |
| Sider (fra-til) | 13-23 |
| Antal sider | 11 |
| ISSN | 0364-5134 |
| DOI | |
| Status | Udgivet - 2021 |
Bibliografisk note
Funding Information:
The binding of pathogenic AQP4‐specific autoantibodies to astrocytes is a key event in the formation of neuromyelitis optica (NMO) lesions. This has been well documented in animal models, and is supported by the pathology of NMO in humans. NMO is an inflammatory demyelinating disease of the CNS caused by binding of pathogenic IgG autoantibodies to AQP4. Astrocyte damage and downstream inflammation require NMO‐IgG effector function to initiate complement‐dependent cytotoxicity (CDC) and antibody‐dependent cell‐mediated cytotoxicity (ADCC). The discovery of AQP4 as a biomarker marked a breakthrough in the understanding of the pathogenesis of the disease. 55–57 58–60
Funding Information:
We thank N. Kim for editorial and graphical assistance, which was funded by the European Charcot Foundation, a nonprofit foundation and organizer of the 27th Annual Meeting at Baveno, Italy, which was sponsored by Biogen, Celgene, MedDay, Merck, Novartis, Roche, Sanofi Genzyme, and Teva.
Funding Information:
We thank N. Kim for editorial and graphical assistance, which was funded by the European Charcot Foundation, a nonprofit foundation and organizer of the 27th Annual Meeting at Baveno, Italy, which was sponsored by Biogen, Celgene, MedDay, Merck, Novartis, Roche, Sanofi Genzyme, and Teva.
Publisher Copyright:
© 2020 American Neurological Association
ID: 270200882