T-independent activation-induced cytidine deaminase expression, class-switch recombination, and antibody production by immature/transitional 1 B cells.
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.
Duke Scholars
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- Toll-Like Receptors
- Spleen
- Plasma Cells
- Mice, Nude
- Mice, Knockout
- Mice
- Lymphopoiesis
- Immunology
- Immunoglobulins
- Immunoglobulin Class Switching
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Toll-Like Receptors
- Spleen
- Plasma Cells
- Mice, Nude
- Mice, Knockout
- Mice
- Lymphopoiesis
- Immunology
- Immunoglobulins
- Immunoglobulin Class Switching