Abstract
Inflammation elicits a splenic lymphopoiesis of unknown physiologic significance but one that juxtaposes developing B cells and exogenous Ag. We show that immature and transitional 1 (immature/T1) B cells constitutively express activation-induced cytidine deaminase and B lymphocyte-induced maturation protein 1 in amounts that support accelerated plasmacytic differentiation and limited class-switch recombination. In vivo, activation of immature/T1 B cells by TLR ligands or bacterial vaccine rapidly induces T1 cells to divide, proliferate, and secrete IgM, IgG, or IgA Ab; in vitro, proliferation and differentiation are substantially enhanced by B cell-activating factor. We propose that inflammation-induced extramedullary lymphopoiesis represents a specialized mechanism for innate Ab responses to microbial pathogens.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Antibody Formation*
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B-Cell Activating Factor / biosynthesis
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B-Cell Activating Factor / immunology
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Bacterial Vaccines / immunology*
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Cell Division / immunology
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Cytidine Deaminase / biosynthesis*
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Cytidine Deaminase / immunology
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Gene Expression Regulation, Enzymologic / immunology*
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Immunity, Innate
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Immunoglobulin Class Switching / immunology*
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Immunoglobulins / biosynthesis
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Immunoglobulins / immunology
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Lymphopoiesis / immunology
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Mice
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Mice, Knockout
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Mice, Nude
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Plasma Cells / immunology*
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Plasma Cells / metabolism
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Spleen / immunology
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Spleen / metabolism
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Toll-Like Receptors / agonists
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Toll-Like Receptors / immunology
Substances
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B-Cell Activating Factor
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Bacterial Vaccines
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Immunoglobulins
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Toll-Like Receptors
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AICDA (activation-induced cytidine deaminase)
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Cytidine Deaminase