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Department of Immunology, Duke University Medical Center, Durham, NC 27710
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.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by National Institutes of Health Grants AI-49326 and AI-24335 and the Duke University Autoimmunity Center of Excellence Grant AI-56363.
2 Address correspondence and reprint requests to Dr. Garnett Kelsoe, Department of Immunology, Box 3010, Duke University Medical Center, Durham, NC 27710. E-mail address: ghkelsoe{at}duke.edu
3 Abbreviations used in this paper: BM, bone marrow; AID, activation-induced cytidine deaminase; AFC, Ab-forming cell; AMuLV, Abelson murine leukemia virus; AP, alkaline phosphatase; BAFF, B cell-activating factor; BLIMP-1, B lymphocyte-induced maturation protein 1; CGG, chicken gammaglobulin; CSR, class-switch recombination; CT, circle transcript; CT, threshold cycle; GC, germinal center; GLT, germline transcript; im, immature; IRAK4, IL-1R-associated kinase 4; LAT, linker of activated T cell; MF, mature follicular; MZ, marginal zone; NP, (4-hydroxy-3-nitrophenyl)acetyl; SA, streptavidin; SHM, somatic hypermutation; T1, translational 1; Tg, transgenic; Ti, T cell independent.
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