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Originally published online as doi:10.1189/jlb.0206096 on August 30, 2006

Published online before print August 30, 2006
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(Journal of Leukocyte Biology. 2006;80:1416-1423.)
© 2006 by Society for Leukocyte Biology

Redundant and unique regulation of activated mouse B lymphocytes by IL-4 and IL-21

Haoli Jin1 and Thomas R. Malek2

Department of Microbiology and Immunology, Miller School of Medicine, University of Miami, Miami, Florida, USA

2 Correspondence: Department of Microbiology and Immunology, University of Miami School of Medicine, P.O. Box 016960, Miami, FL 33101, USA. E-mail: tmalek{at}med.miami.edu

IL-21 distinctively regulates B cell growth and death, and it redundantly functions with IL-4 for IgG production. B cells likely encounter IL-4 and IL-21 in vivo, as both are secreted by activated T cells. Therefore, the action of both these cytokines was investigated during activation of B cells. IL-21 or the combination of IL-4 and IL-21 inhibited proliferation by purified mouse B cells to LPS or CpG DNA, whereas these cytokines enhanced proliferation after engaging the BCR or CD40. Although B cell subsets expressed somewhat varied levels of the IL-21 receptor, LPS-stimulated follicular and marginal B cell subsets were also dominantly susceptible to IL-21-induced growth arrest and cell death. After activation of B cells with CD40 and LPS, IL-4 and IL-21 distinctively regulated the expression of CD23, CD44, and CD138, and they cooperatively promoted IgG1 class-switching and synthesis. These findings support a model in which the presence of IL-4 and IL-21 inhibits B cells activated by polyclonal innate signals, and they promote B cell expansion and differentiation during T cell-dependent antibody responses, although the individual responses to IL-4 and IL-21 do not always overlap.

Key Words: apoptosis • costimulation




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