B-cell depletion with rituximab in relapsing-remitting multiple sclerosis
By D. Bourdette, V. Yadav. Current Neurology and Neuroscience Reports, 2008
1,132 citations recorded by the source corpus.
Subfields: Immunology, Neurology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/502626bc46f139312a581fa7edd7afa878fc930c
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Citations in the corpus
- Cellular and synaptic mechanisms of anti-NMDA receptor encephalitis (2010, background): “As postulated in other disorders, these cells are able to cross the blood-brain-barrier, and are believed to undergo restimulation, antigen-driven affinity maturation, clonal expansion, and differentiation into antibody-secreting plasma cells(Hauser et al., 2008).”
- Regulatory B cells inhibit EAE initiation in mice while other B cells promote disease progression. (2008, background): “A recent phase II trial using rituximab has suggested clinical efficacy in MS patients (25); however, the mechanisms underlying the effect of B cell depletion on disease activity remain unknown.”
- Efficacy and safety of rituximab in patients with active proliferative lupus nephritis: the Lupus Nephritis Assessment with Rituximab study. (2012, neutral): “treatment of relapsing-remitting multiple sclerosis (17)”
- EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2016 update (2010, neutral): “Until then we hope that the 2016 update will be broadly applied in clinical practice and/or serve as a template for national societies to develop local recommendations.”
- T follicular helper cell differentiation, function, and roles in disease (2014, background): “…that is nurturing for other immunological cell types with more direct roles in affecting disease progression or regression, whether they be CTL in the context to tumor immunity (Bindea et al., 2013; Gu-Trantien et al., 2013) or Th17 cells in the context of multiple sclerosis (Hauser et al., 2008).”