No role of interleukin-4 in CD23DgE-mediated enhancement of the murine antibody response in vivo
Antigen-specific IgE up-regulates the specific IgM, IgG1, IgG2a and IgE response in vivo when given to mice together with antigen. The enhancement is mediated by the low-affinity receptor for IgE, FceRII or CD23, as demonstrated both in CD23-deficient mice and by blocking CD23 with anti-CD23 monoclonal antibodies. A possible mechanism behind the regulatory effects of CD23 is that the IgE/CD23/antigen complex is endocytosed by B cells, leading to increased antigen processing and presentation on major histocompatibility complex (MHC) class I1 molecules to T helper cells. In the present study we have found that the expression of CD23 is reduced fivefold on splenic Bcells in mice genetically deficient for IL-4. When IL-Cdeficient mice and normal littermates were immunized with 2,4,6-trinitrophenyl (TNP)-specific IgE followed by bovine serum albumin (BSA)-TNP or with BSA-TNP alone, the BSA-specific IgGl and IgG2a responses were equally well augmented by IgE in all mice. In addition, a low but significant IgE response was seen even in the IL-Cdeficient mice. Thus, enhancement of the antibody response through IgE and CD23 occur in the absence of IL-4 and is not dependent on CD23 up-regulation.