Abstract
B cells play diverse and fundamental roles in the pathogenesis of autoimmune diseases. Consequently, therapeutic targeting of B cells is gaining prominence in our clinical armamentarium for an ever expanding array of autoimmune and neoplastic disorders. Therefore, it is of great importance to understand the mechanism of action of B cell depletion. Given that the ideal consequence of B cell depletion would be the subsequent re-establishment of immunologic tolerance, a detailed analysis of the properties of the emerging repertoire will be required. The results presented by Rouzière and coworkers in their study of rheumatoid arthritis patients shed some light on this question and are discussed in this commentary.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Comment
MeSH terms
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Adult
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal / therapeutic use*
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Antibodies, Monoclonal, Murine-Derived
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Antigens, CD19 / analysis
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Arthritis, Rheumatoid / drug therapy
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Arthritis, Rheumatoid / immunology*
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Autoimmune Diseases / drug therapy
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Autoimmune Diseases / immunology*
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B-Lymphocyte Subsets / immunology
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B-Lymphocyte Subsets / pathology*
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Gene Rearrangement, B-Lymphocyte, Heavy Chain
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Hematopoiesis
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Humans
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Immunoglobulin G / genetics
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Immunoglobulin M / genetics
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Immunophenotyping
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Lymphocyte Depletion
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Polymerase Chain Reaction
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Rituximab
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Somatic Hypermutation, Immunoglobulin
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Tumor Necrosis Factor Receptor Superfamily, Member 7 / analysis
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Murine-Derived
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Antigens, CD19
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Immunoglobulin G
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Immunoglobulin M
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Tumor Necrosis Factor Receptor Superfamily, Member 7
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Rituximab