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The Journal of Immunology, 2005, 175: 1286-1294.
Copyright © 2005 by The American Association of Immunologists

Hom s 4, an IgE-Reactive Autoantigen Belonging to a New Subfamily of Calcium-Binding Proteins, Can Induce Th Cell Type 1-Mediated Autoreactivity1

Karl J. Aichberger*,¶, Irene Mittermann*, Renate Reininger{dagger}, Susanne Seiberler*, Ines Swoboda{dagger}, Susanne Spitzauer{dagger}, Tamara Kopp{ddagger}, Georg Stingl{ddagger}, Wolfgang R. Sperr, Peter Valent, Andreas Repa§, Barbara Bohle*, Dietrich Kraft* and Rudolf Valenta2,*

* Division of Immunopathology, Department of Pathophysiology, Center for Physiology and Pathophysiology,{dagger} Clinical Institute for Medical and Chemical Laboratory Diagnostics,{ddagger} Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology,§ Division of Neonatology and Intensive Care, Department of Pediatrics, and Division of Hematology and Hemostaseology, Department of Internal Medicine I, Vienna General Hospital, Medical University of Vienna, Austria

Skin inflammation in atopic dermatitis starts with Th2 and IgE-mediated responses against exogenous allergens and, for unknown reasons, resembles features of a Th1-driven reaction in the chronic stages. We report the characterization of a human protein, Hom s 4, recognized by IgE autoantibodies from atopic dermatitis patients. The complete Hom s 4 cDNA codes for a 54-kDa basic protein containing two typical calcium-binding domains separated by an unusually long {alpha}-helical domain. Therefore, Hom s 4 and homologous proteins found by sequence comparison in mice, fruit flies, and nematodes constitute a novel subfamily of calcium-binding proteins. Using Hom s 4-specific Abs, it is demonstrated that the protein is strongly expressed within epidermal keratinocytes and dermal endothelial cells. Purified Hom s 4 showed IgE cross-reactivity with exogenous calcium-binding allergens from plants and fish but, in contrast to the exogenous allergens, induced only weak histamine release from patient basophils. However, the analysis of Hom s 4-specific cytokine and humoral immune responses indicated that Hom s 4 strongly induces Th1 responses which are accompanied by the release of IFN-{gamma}, a cytokine implicated in epithelial cell damage. Hom s 4-induced IFN-{gamma} production was found in normal individuals, in patients with chronic inflammatory skin diseases and in Th2-prone atopic persons, suggesting that Hom s 4 represents a protein with an intrinsic property to induce Th1-mediated autoreactivity. It may thus contribute to chronic skin inflammation in atopic as well as in nonatopic persons.




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