1. ^*Institute of General and Experimental Pathology, Vienna, Austria
2. ^†Department of Dermatology, Division of Allergy, Immunology and Infectious Diseases, Vienna, Austria
3. ^‡Department of Internal Medicine I, Division of Hematology and Hemostasiology, Vienna General Hospital, University of Vienna Medical School, Vienna, Austria
4. ^§Institute of Histology and Embryology, University of Innsbruck Medical School, Innsbruck, Austria
5. ^¶Institute of Biotechnology, University of Helsinki, Helsinki, Finland
6. ^††Institute of Developmental Biology, University of Salzburg, Salzburg, Austria
7. ^**Institute of Medical Physics, University of Münster Medical School, Münster, Germany

Correspondence: Dr Rudolf Valenta, Institute of General and Experimental Pathology, Vienna General Hospital, University of Vienna Medical School, Waehringer Guertel 18-20, A-1090 Vienna, Austria

²Susanne Natter and Susanne Seiberler contributed equally to the work and are listed in alphabetical order.

¹Part of this manuscript was previously published in the proceedings of the 21st Symposium of the Collegium Internationale Allergologicum "Allergy – A Disease of Modern Society", Int Arch Allergy Immunol 113:209–212, 1998.

Received 9 June 1998; Accepted 4 August 1998.

Abstract

Atopy is a genetically determined disorder that affects 10%–20% of the population. Many symptoms of patients with atopy (allergic rhinitis, conjunctivitis, asthma, and anaphylaxis) result from events occurring after cross-linking of cell-bound IgE by per se innocuous environmental antigens. The frequently raised hypothesis that autosensitization can also be a pathogenetic factor in atopy, gained support by our recent demonstration of IgE antibodies against human proteins in atopic dermatitis patients. To unravel the molecular nature of IgE-defined autoantigens, we used serum IgE from atopic dermatitis patients to screen a human epithelial cDNA expression library. One of the cDNA-encoding IgE-reactive products contained 1501 bp of a 2274 bp open-reading frame finally identified by sequence analysis of two additional cDNA clones resulting from oligonucleotide screening. The IgE-defined autoantigen, designated Hom s 1, exhibited an almost complete sequence identity with a recently described antigen recognized by cytotoxic T cells of a squamous cell carcinoma patient. Purified recombinant Hom s 1specifically bound IgE from patients with severe atopy. When used as immunogen in rabbits, recombinant Hom s 1 gave rise to an anti-serum that reacted with a cytoplasmic protein exhibiting a broad cellular and tissue reactivity (skin, lung >> gastrointestinal tract >> muscle, brain) and identified a 55 kDa protein in blotted serum IgE preparations. The attractive possibility remains that the Hom s 1-triggered IgE response contributes to the events resulting in allergic tissue inflammation. If so, the respective recombinant molecule may serve as a paradigmatic tool for the diagnosis and treatment of patients with "intrinsic" atopy.