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Redundant and unique regulation of activated mouse B lymphocytes by IL‐4 and IL‐21
Author(s) -
Jin Haoli,
Malek Thomas R.
Publication year - 2006
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0206096
Subject(s) - biology , b cell , cd40 , microbiology and biotechnology , naive b cell , cd23 , interleukin 4 , b 1 cell , programmed cell death , t cell , immunology , apoptosis , antibody , cytokine , antigen presenting cell , immune system , cytotoxic t cell , in vitro , immunoglobulin e , biochemistry
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.