Abstract
B cells play central roles in pathogenesis of SLE through autoantibody production, autoantigen-presentation, cytokine production and activation of cognate T cells. Recently, a specific subset of B cells, which exerts immunoregulatory properties via IL-10 production was identified, and dysfunction of these B cells might involved in the pathogenesis of SLE. Currently, various therapies targeting B cells, such as B cell-depletive therapy and B cell regulation molecules seems promising, however, their efficacy and safety in the treatment of SLE should be carefully verified in the future. Because the pathogenesis varies in each patients with SLE, the advent of new era in which therapies can be selected based on an individual immune abnormality is waiting.
MeSH terms
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Aminopyridines
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Antibodies, Monoclonal, Humanized / therapeutic use
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Antibodies, Monoclonal, Murine-Derived / therapeutic use
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Autoimmunity
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B-Cell Activating Factor / biosynthesis
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B-Lymphocyte Subsets / immunology*
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Clinical Trials as Topic
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Humans
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Interleukin-10 / biosynthesis
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Lupus Erythematosus, Systemic / drug therapy
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Lupus Erythematosus, Systemic / immunology*
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Lupus Erythematosus, Systemic / therapy
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Lymphocyte Activation
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Lymphocyte Depletion / methods
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Molecular Targeted Therapy
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Morpholines
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Oxazines / therapeutic use
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Pyridines / therapeutic use
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Pyrimidines
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Rituximab
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T-Lymphocytes / immunology
Substances
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Aminopyridines
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Antibodies, Monoclonal, Humanized
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Antibodies, Monoclonal, Murine-Derived
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B-Cell Activating Factor
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Morpholines
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Oxazines
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Pyridines
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Pyrimidines
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Interleukin-10
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epratuzumab
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Rituximab
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belimumab
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fostamatinib