Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-15834
Mittermann, I; Reininger, R; Zimmermann, M; Gangl, K; Reisinger, J; Aichberger, K J; Greisenegger, E K; Niederberger, V; Seipelt, J; Bohle, B; Kopp, T; Akdis, C A; Spitzauer, S; Valent, P; Valenta, R (2008). The IgE-reactive autoantigen Hom s 2 induces damage of respiratory epithelial cells and keratinocytes via induction of IFN-gamma. Journal of Investigative Dermatology, 128(6):1451-1459.
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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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|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Swiss Institute of Allergy and Asthma Research|
|Dewey Decimal Classification:||610 Medicine & health|
|Deposited On:||24 Feb 2009 13:02|
|Last Modified:||22 Oct 2014 11:13|
|Publisher:||Nature Publishing Group|
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