Abstract
BLyS and APRIL have similar but distinct biological roles, mediated through two known TNF receptor family members, TACI and BCMA. We show that mice treated with TACI-Ig and TACI-Ig transgenic mice have fewer transitional T2 and mature B cells and reduced levels of circulating immunoglobulin. TACI-Ig treatment inhibits both the production of collagen-specific Abs and the progression of disease in a mouse model of rheumatoid arthritis. In BLyS-deficient mice, B cell development is blocked at the transitional T1 stage such that virtually no mature B cells are present, while B-1 cell numbers are relatively normal. These findings further elucidate the roles of BLyS and APRIL in modulating B cell development and suggest that BLyS is required for the development of most but not all mature B cell populations found in the periphery.
MeSH terms
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Animals
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Antibody Formation
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Arthritis, Rheumatoid / etiology
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Arthritis, Rheumatoid / immunology
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Autoantibodies / blood
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Autoimmune Diseases / etiology*
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B-Cell Activation Factor Receptor
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B-Lymphocytes / classification
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B-Lymphocytes / immunology*
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Cell Differentiation
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Cell Lineage
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Collagen / immunology
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Homozygote
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Immunoglobulins / blood
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Membrane Proteins*
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Mice
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Mice, Transgenic
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Phenotype
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Receptors, Tumor Necrosis Factor / genetics
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Receptors, Tumor Necrosis Factor / immunology
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Receptors, Tumor Necrosis Factor / metabolism*
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Transmembrane Activator and CAML Interactor Protein
Substances
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Autoantibodies
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B-Cell Activation Factor Receptor
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BLyS receptor
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Immunoglobulins
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Membrane Proteins
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Receptors, Tumor Necrosis Factor
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Tnfrsf13b protein, mouse
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Tnfrsf13c protein, mouse
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Transmembrane Activator and CAML Interactor Protein
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Collagen