No role of interleukin‐4 in CD23/IgE‐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, FcϵRII 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 II molecules toT helper cells. In the present study we have found that the expression of CD23 is reduced fivefold on splenic B cells in mice genetically deficient for IL‐4. When IL‐4‐deficient 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 IgG1 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‐4‐deficient 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.