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The IgE-reactive Autoantigen Hom S 2 Induces Damage Of Respiratory Epithelial Cells And Keratinocytes Via Induction Of IFN-gamma.
I. Mittermann, R. Reininger, M. Zimmermann, K. Gangl, J. Reisinger, K. Aichberger, Elli K. Greisenegger, V. Niederberger, J. Seipelt, B. Bohle, T. Kopp, C. Akdis, S. Spitzauer, P. Valent, R. Valenta
Published 2008 · Medicine
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Hom s 2, the alpha-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-gamma in cultured peripheral blood mononuclear cells from atopic as well as non-atopic individuals. IFN-gamma-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-gamma antibody. Our data demonstrate that the Hom s 2 autoantigen can cause IFN-gamma-mediated cell damage.
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