| First Author | Jin H | Year | 2006 |
| Journal | J Leukoc Biol | Volume | 80 |
| Issue | 6 | Pages | 1416-23 |
| PubMed ID | 16943384 | Mgi Jnum | J:116595 |
| Mgi Id | MGI:3694545 | Doi | 10.1189/jlb.0206096 |
| Citation | Jin H, et al. (2006) Redundant and unique regulation of activated mouse B lymphocytes by IL-4 and IL-21. J Leukoc Biol 80(6):1416-23 |
| abstractText | 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. |
