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- Title
Ig E knock-in mice suggest a role for high levels of Ig E in basophil-mediated active systemic anaphylaxis.
- Authors
Lübben, Wolger; Turqueti‐Neves, Adriana; Okhrimenko, Anna; Stöberl, Christian; Schmidt, Volker; Pfeffer, Klaus; Dehnert, Sonja; Wünsche, Sarah; Storsberg, Silke; Paul, Stefanie; Bauer, Stefan; Riethmüller, Gert; Voehringer, David; Yu, Philipp
- Abstract
Immunglobulin E ( Ig E) production is tightly regulated at the cellular and genetic levels and is believed to be central to allergy development. At least two cellular pathways exist that lead to systemic anaphylaxis reactions in vivo: Ig E-sensitized mast cells and Ig G1-sensitized basophils. Passive anaphylaxis, by application of allergen and allergen-specific antibodies in mice, indicates a differential contribution of immunoglobulin isotypes to anaphylaxis. However, analysis of a dynamic immunization-mediated antibody response in anaphylaxis is difficult. Here, we generated Ig E knock-in mice ( Ig Eki), which express the Ig E heavy chain instead of Ig G1, in order to analyze the contribution of Ig G1 and Ig E to active anaphylaxis in vivo. Ig Eki mice display increased Ig E production both in vitro and in vivo. The sensitization of Ig Eki mice by immunization followed by antigen challenge leads to increased anaphylaxis. Homozygous Ig Eki mice, which lack Ig G1 due to the knock-in strategy, are most susceptible to active systemic anaphylaxis. The depletion of basophils demonstrates their importance in Ig E-mediated anaphylaxis. Therefore, we propose that an enhanced, antigen-specific, polyclonal Ig E response, as is the case in allergic patients, is probably the most efficient way to sensitize basophils to contribute to systemic anaphylaxis in vivo.
- Publication
European Journal of Immunology, 2013, Vol 43, Issue 5, p1231
- ISSN
0014-2980
- Publication type
Article
- DOI
10.1002/eji.201242675