Cutting edge: Helminth infection induces IgE in the absence of μ- or δ-chain expression

Georgia Perona-Wright, Katja Mohrs, Justin Taylor, Colby Zaph, David Artis, Edward J. Pearce, Markus Mohrs

Research output: Contribution to journalArticleResearchpeer-review

21 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)6697-6701
Number of pages5
JournalJournal of Immunology
Volume181
Issue number10
Publication statusPublished - 15 Nov 2008
Externally publishedYes

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