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T-independent activation-induced cytidine deaminase expression, class-switch recombination, and antibody production

Yoshihiro Ueda1, Dongmei Liao, Kaiyong Yang

  • 1Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|March 7, 2007
PubMed

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.

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