Infections with helminth parasites are associated with an IgE isotype switch and high serum IgE concentrations. IgE is rapidly bound by the high affinity IgE receptor (FcεRI), thereby sensitizing FcεRI-bearing basophils and mast cells for IgE-inducible effector functions such as IL-4 production. The development of Absecreting B cells is dependent on IgM and consequently, μMT mice, which lack surface IgM, are considered devoid of Abs. In this study we report the unexpected finding that C57BL/6 μMT mice generate robust IgE responses upon infection with three distinct helminth parasites, Heligmosomoides polygyrus, Trichuris muris, and Schistosoma mansoni. IgE is produced despite an apparent block in B cell development and licenses basophils for IgE-induced IL-4 production. Our findings reveal the existence of an evolutionarily conserved, IgM-independent pathway for the production of IgE upon infection with helminth parasites.
|Number of pages||5|
|Journal||Journal of Immunology|
|Publication status||Published - 15 Nov 2008|