IL-4 (B cell stimulatory factor 1) overcomes Fc gamma receptor-mediated inhibition of mouse B lymphocyte proliferation without affecting inhibition of c-myc mRNA induction
Autor: | N E, Phillips, K A, Gravel, K, Tumas, D C, Parker |
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Rok vydání: | 1988 |
Předmět: |
B-Lymphocytes
Cell-Free System Interleukins Receptors IgG Receptors Antigen B-Cell Receptors Fc T-Lymphocytes Helper-Inducer Lymphocyte Activation Antigens Differentiation Binding Competitive Antibodies Anti-Idiotypic Cell Line Proto-Oncogene Proteins c-myc Mice Cross-Linking Reagents Immunoglobulin M Mice Inbred DBA Immunoglobulin G Proto-Oncogene Proteins Concanavalin A Animals Female Interleukin-4 RNA Messenger |
Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 141(12) |
ISSN: | 0022-1767 |
Popis: | 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 Fc gamma R on B cells. This report describes conditions under which IgG anti-mu or anti-delta will induce proliferation despite Fc gamma R 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 Fc gamma R, also proliferate to IgG anti-Ig. We have previously shown that Fc gamma R-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. |
Databáze: | OpenAIRE |
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