Publications

Abstract

The selection of an appropriate immunoglobulin (Ig) isotype is critical for an effective immune response against pathogens. Isotype regulation is sensitive to external signals, particularly cytokines secreted by T helper cells. For example, interleukin (IL)-4 induces isotype switching to IgG1 via a STAT6-dependent signalling pathway. Here, we show that B cell receptor (BCR) ligation also induces IgG1 switching. The extent of switch induction by antigen is affinity-dependent and high affinity antigen binding leads to IgG1 switching levels comparable to those induced by saturating IL-4. However, the antigen-induced IgG1 switch does not require additional cytokine signals and occurs in a STAT6-independent manner. Thus, BCR ligation represents a novel pathway for direct isotype switching leading to IgG1 secretion.