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

Haoli Jin, Thomas Malek

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1416-1423
Number of pages8
JournalJournal of Leukocyte Biology
Volume80
Issue number6
DOIs
StatePublished - Dec 1 2006

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Interleukin-4
B-Lymphocytes
B-Lymphocyte Subsets
Interleukin-21 Receptors
Cell Death
Immunoglobulin G
Immunoglobulin Class Switching
Cytokines
T-Lymphocytes
interleukin-21
Growth
Antibody Formation
Cell Differentiation
DNA

Keywords

  • Apoptosis
  • Costimulation

ASJC Scopus subject areas

  • Cell Biology

Cite this

Redundant and unique regulation of activated mouse B lymphocytes by IL-4 and IL-21. / Jin, Haoli; Malek, Thomas.

In: Journal of Leukocyte Biology, Vol. 80, No. 6, 01.12.2006, p. 1416-1423.

Research output: Contribution to journalArticle

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