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 language | English (US) |
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Pages (from-to) | 4243-4349 |
Number of pages | 107 |
Journal | Journal of Immunology |
Volume | 141 |
Issue number | 12 |
State | Published - 1988 |
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology