期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 6, 页码 3593-3601出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.6.3593
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资金
- NIAID NIH HHS [R01 AI024335-21, R01 AI049326, U19 AI056363, U19 AI056363-010002, AI 24335, AI 56363, R01 AI024335, AI 49326] Funding Source: Medline
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 Journal of Immunology, 2007, 178: 3593-3601.
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