IL-4 (B cell stimulatory factor 1) overcomes Fcγ receptor-mediated inhibition of mouse B lymphocyte proliferation without affecting inhibition of c-myc mRNA induction

N. E. Phillips, K. A. Gravel, K. Tumas, D. C. Parker

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

Mouse B cells are stimulated to proliferate by Fab'2 fragments of rabbit anti-mouse Ig antibodies. Proliferation is inhibited, however, in the presence of IgG anti-mouse Ig. We have previously shown that this inhibition is mediated by binding of the IgG anti-Ig to receptors for FcγR on B cells. This report describes conditions under which IgG anti-μ or anti-δ will induce proliferation despite FcγR engagement. Culture supernatants of Con A-stimulated, Il-4-secreting Th cell lines, but not of Il-2-secreting Th cell lines, will co-stimulate with IgG anti-Ig to induce small B cells to incorporate [3H]TdR. This co-mitogenic activity is inhibitable by anti-IL-4 antibodies and can also be induced by Il-4 affinity purified from the T cell supernatants or by supernatants containing rIl-4. B cells precultured with Il-4 for 18 h, while still expressing normal levels of FcγR, also proliferate to IgG anti-Ig. We have previously shown that FcγR-mIg cross-linking will inhibit mIg-dependent increases in c-myc mRNA levels. We investigated whether Il-4 allows B cells to respond to IgG anti-Ig by elevating c-myc. The data show that Il-4 has little effect on c-myc mRNA levels in either IgG or Fab'2 anti-Ig-containing cultures.

Original languageEnglish (US)
Pages (from-to)4243-4349
Number of pages107
JournalJournal of Immunology
Volume141
Issue number12
StatePublished - Dec 1 1988

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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