Premium
IgE‐binding components of cultured human keratinocytes in atopic eczema/dermatitis syndrome and their crossreactivity with Malassezia furfur
Author(s) -
KortekangasSavolainen O.,
Peltonen S.,
Pummi K.,
Kalimo K.,
Savolainen J.
Publication year - 2004
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1046/j.1398-9995.2003.00330.x
Subject(s) - immunoglobulin e , atopic dermatitis , immunology , radioallergosorbent test , malassezia , allergy , antibody , epitope , hypoallergenic , medicine , allergen , biology , microbiology and biotechnology
Background: Atopic eczema/dermatitis syndrome (AEDS) patients display immunoglobulin E (IgE) reactivity to several antigens, e.g. saprophytic yeasts as Malassezia furfur . AEDS patients also show IgE autoreactivity towards cells of their own tissue including epidermis. Purpose of the study: The aim of this study was to investigate the IgE autoreactivity of AEDS patients to cultured keratinocytes and to reveal potential crossreacting epitopes in cultured keratinocytes and M. furfur . Material and methods: Serum samples of 27 AEDS patients were analyzed, of these 13 were M. furfur radioallergosorbent test (RAST) positive and 14 negative. Four urticaria, three psoriasis, and seven nonatopic patients were included as controls. The studies were performed by using IgE immunoblotting and immunoblotting inhibition methods. Results: Ten IgE‐binding protein bands were detected in cultured human keratinocytes by IgE immunoblotting using sera from adult AEDS patients. Anti‐keratinocyte IgE antibodies were more associated with elevated S‐IgE level than M. furfur RAST. Clear crossreactivity with M. furfur could not be shown. Conclusions: The possible pathomechanism of anti‐keratinocyte IgE antibodies is not due to IgE epitope mimicry of saprophytic yeast and local tissue in AEDS skin.