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On the role of antibody affinity in the IgE mediated allergic response
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  • Monique Vogel,
  • Martin Bachmann,
  • Mona O. Mohsen,
  • Matthias Kramer,
  • Sviatlana Starchenka,
  • Piers Whitehead,
  • Matthew Heath
Monique Vogel
Universitat Bern
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Martin Bachmann
Universitat Bern

Corresponding Author:martin.bachmann@dbmr.unibe.ch

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Mona O. Mohsen
Universitat Bern
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Matthias Kramer
Bencard Allergie GmbH
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Sviatlana Starchenka
Allergy Therapeutics Plc
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Piers Whitehead
Bencard Allergie GmbH
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Matthew Heath
Allergy Therapeutics Plc
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Abstract

Type I hypersensitivity, also known as classical allergy, is mediated via allergen-specific IgE antibodies bound to type I FcR (FcεRI) on the surface of mast cells and basophils upon cross-linking by allergens. This IgE-mediated cellular activation may be blocked by allergen-specific IgG through multiple mechanisms, including direct neutralization of the allergen or engagement of the inhibitory receptor FcγRIIb which blocks IgE signal transduction. In addition, co-engagement of FceRI and FcγRIIb by IgE-IgG-allergen immune-complexes causes down-regulation of receptor bound IgE, resulting in desensitization of the cells. Both, activation of FceRI by allergen-specific IgE and engagement of FcγRIIb by allergen-specific IgG are driven by allergen-binding. Here we delineate the distinct roles of antibody affinity versus avidity in driving these processes and discuss the role of IgG subclasses in inhibiting basophil and mast cell activation.