Abstract

Abstract Histamine is a critical mediator of allergic disease and signals through four receptors. We recently showed that histamine 2 receptor (H2R) is essential for IL-4 mediated eosinophil recruitment and that H2R deficient mice are protected from allergic airway inflammation. Additionally, we observed an inability to generate IgE in these mice. This was not due to a sensitization defect, since the mice are capable of generating antigen specific IgG1. However, the functions of H2R on B cells are unclear. Here we show that H2R is not required for B cell development and proliferation and that H2R deficient mice are capable of generating antibodies to the T independent antigens NP FICOLL and NP LPS. However, H2R deficient B cells were unable to class-switch to IgE in vitro. This was further characterized by an absence of epsilon specific post-switch transcripts in H2R deficient B cells. The upregulation of CD23 in response to IL-4 was also impaired in H2R deficient B cells. STAT6 phosphorylation in IL-4 treated B cells from H2R deficient mice was also reduced. These findings suggest that histamine is vital in permitting IL-4 signaling to mediate STAT6 phosphorylation and for the switch to IgE that occurs in B cells.

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