Interleukin‐3‐treated non‐B, non‐T cells switch activated B cells to IgG1/IgE synthesis

摘要

AbstractThe switch of activated B cells to IgE synthesis is an interleukin (IL)‐3‐dependent process. It is currently thought that specific T cells activated by antigen presented in the context of class II major histocompatibility complex are the major source of IL‐4. Recently it has been demonstrated that a splenic non‐T non‐B cell population (termed NBNT) has the capacity to produce IL‐4 following IgE and IgG receptor cross‐linkage. In this study we demonstrate that IL‐4 producing NBNT cells can induce the switch of lipopolysaccharide‐activated B cells to the synthesis of IgG1and IgE antibodies. Furthermore, it was found that not only IgE receptor cross‐linkage but IL‐3 was able to stimulate NBNT cells to produce IL‐4 and induce the switch of B cells to IgE synthesis. NBNT cells derived from the spleen and bone marrow of SCID mice were able to produce IL‐4 on exposure to IL‐3. This suggested that the ability of IL‐3 to stimulate IL‐4 production was not dependent on prior exposure of the NBNT cells to antibody complexesin vivo. Taken together these findings represent the first observation that enough IL‐4 is produced by NBNT cells to actually influence a B cell IgG/Ig response. The findings also clearly demonstrate that B cells do not need high concentrations of IL‐4 to be directed