1. ¹Division of Immunopathology, Department of Pathophysiology, Center for Physiology and Pathophysiology, Medical University of Vienna, Vienna, Austria
2. ²Clinical Institute for Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria
3. ³Swiss Institute of Allergy and Asthma Research, Davos, Switzerland
4. ⁴Department of Otorhinolaryngology, Medical University of Vienna, Vienna, Austria
5. ⁵Division of Hematology and Hemostaseology, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria
6. ⁶Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, Medical University of Vienna, Vienna, Austria
7. ⁷Max F. Perutz Laboratories, Medical University of Vienna, Vienna, Austria

Correspondence: Professor Rudolf Valenta, Division of Immunopathology, Department of Pathophysiology, Center for Physiology and Pathophysiology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna A-1090, Austria. E-mail: rudolf.valenta@meduniwien.ac.at

Received 21 December 2006; Revised 14 September 2007; Accepted 26 September 2007; Published online 13 December 2007.

Abstract

Hom s 2, the -chain of the nascent polypeptide-associated complex, is an intracellular autoantigen that has been identified with IgE autoantibodies from atopic dermatitis patients. We investigated the humoral and cellular immune response to purified recombinant Hom s 2 (rHom s 2). rHom s 2 exhibited IgE reactivity comparable to exogenous allergens, but did not induce relevant basophil cell degranulation. The latter may be attributed to the fact that patients recognized single epitopes on Hom s 2 as revealed by IgE epitope mapping with rHom s 2 fragments. In contrast to exogenous allergens, rHom s 2 had the intrinsic ability to induce the release of IFN- in cultured peripheral blood mononuclear cells from atopic as well as non-atopic individuals. IFN--containing culture supernatants from Hom s 2-stimulated peripheral blood mononuclear cells caused disintegration of respiratory epithelial cell layers and apoptosis of skin keratinocytes, which could be inhibited with a neutralizing anti-IFN- antibody. Our data demonstrate that the Hom s 2 autoantigen can cause IFN--mediated cell damage.