CD40 signaling induces interleukin‐4‐independent IgE switching in vivo

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Abstract
T cell‐deficient T cell receptor (TCR) β−/− x TCR δ−/− knockout mice lack circulating IgE and fail to produce antigen‐specific IgE in response to stimulation with T cell‐dependent antigens. We show here that these animals are able to produce significant levels of circulating polyclonal IgE when injected with an agonistic anti‐mouse CD40 monoclonal antibody. CD40‐mediated induction of circulating polyclonal IgE in T cell‐deficient mice was only partially reduced when the animals were co‐treated with neutralizing anti‐interleukin‐4 (IL‐4) antibody. The IL‐4 independence of this response was further supported by experiments showing that anti‐CD40 antibodies induced circulating IgE when injected into IL‐4 knockout mice, and sterile RNA ϵ transcript production when cultured with purified B cells from the same mice. These data strongly suggest that CD40 signaling causes IL‐4‐independent IgE switching in mice.