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Department of Biosciences, School of Science, Kitasato University, Kanagawa 228, Japan; and the Department of Molecular Genetics, Faculty of Medicine, Kyoto University, Kyoto 606-8507, Japan
Mouse germinal center (GC) B cells have been shown to undergo secondary V(D)J (V, variable; D, diversity; J, joining) recombination (receptor editing) mediated by the reexpressed products of recombination activating gene (RAG)-1 and RAG-2. We show here that interleukin (IL)-7 as well as IL-4 was effective in inducing functional RAG products in mouse IgD+ B cells activated via CD40 in vitro. Blocking of the IL-7 receptor (IL-7R) by injecting an anti– IL-7R monoclonal antibody resulted in a marked suppression of the reexpression of RAG-2 and subsequent V(D)J recombination in the draining lymph node of immunized mice, whereas RAG-2 expression was not impaired in immunized IL-4–deficient mice. Further, these peripheral B cells activated in vitro or in vivo were found to express IL-7R. These findings indicate a novel role for IL-7 and IL-7R in inducing receptor editing in GC B cells.
Key Words: recombination activating genes • mature B cells • germinal center • interleukin 7 • interleukin 7 receptor
Abbreviations used: D, diversity; FDC, follicular dendritic cell; 
c, the common chain of IL-7R; GC, germinal center; J, joining; RAG or RAG, recombination activating gene; RT-PCR, reverse transcriptase– dependent PCR; V, variable.
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