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dc.contributor.authorBodvarsson, S
dc.contributor.authorJonsdottir, I
dc.contributor.authorFreysdottir, J
dc.contributor.authorLeonard, J N
dc.contributor.authorFry, L
dc.contributor.authorValdimarsson, H
dc.date.accessioned2011-02-16T11:49:47Z
dc.date.available2011-02-16T11:49:47Z
dc.date.issued1993-12
dc.date.submitted2011-02-16
dc.identifier.citationScand. J. Immunol. 1993, 38(6):546-50en
dc.identifier.issn0300-9475
dc.identifier.pmid8256113
dc.identifier.doi10.1111/j.1365-3083.1993.tb03239.x
dc.identifier.urihttp://hdl.handle.net/2336/122058
dc.descriptionTo access publisher full text version of this article. Please click on the hyperlink in Additional Links fielden
dc.description.abstractDermatitis herpetiformis (DH), is associated with skin eruptions and granular depositions of IgA in the papillary dermis, but this is not a feature of coeliac disease (CD). The specificity of the IgA in the skin is unknown. High molecular weight glutenin (HMW-g), a component of gluten, has been shown to have structural similarities to human elastin. This paper reports immunoadsorption studies which suggest that human serum may contain antibodies which cross-react with HMW-g and elastin. DH patients had significantly lower levels of IgA antibodies to HMW-g and to elastin than both CD patients and healthy controls. Furthermore, introduction of a gluten-free diet (GFD) was associated with a further reduction in the amount of IgA antibodies to elastin in the DH patients. This diet-associated decrease of elastin antibodies was restricted to the IgA isotype. A significant correlation was observed between IgA antibodies to HMW-g and elastin in healthy controls and CD patients, while no such correlation was found in patients with DH. These findings could indicate that HMW-g induces production of antibodies to elastin, which are deposited in the skin, and that when the antigenic stimulus is removed, these antibodies are further reduced due to continuous dermal deposition. It is postulated that DH may be an autoimmune disease due to cross-reactivity between dietary glutenin and dermal elastin.
dc.language.isoenen
dc.publisherBlackwell Scientific Publicationsen
dc.relation.urlhttp://dx.doi.org/10.1111/j.1365-3083.1993.tb03239.xen
dc.subject.meshAdulten
dc.subject.meshAutoantibodiesen
dc.subject.meshAutoimmune Diseasesen
dc.subject.meshCeliac Diseaseen
dc.subject.meshCross Reactionsen
dc.subject.meshDermatitis Herpetiformisen
dc.subject.meshDieten
dc.subject.meshElastinen
dc.subject.meshEnzyme-Linked Immunosorbent Assayen
dc.subject.meshGlutensen
dc.subject.meshHumansen
dc.subject.meshImmunoglobulin Aen
dc.subject.meshImmunoglobulin Gen
dc.subject.meshMiddle Ageden
dc.subject.meshSkinen
dc.subject.meshTriticumen
dc.titleDermatitis herpetiformis - an autoimmune disease due to cross-reaction between dietary glutenin and dermal elastin?en
dc.typeArticleen
dc.contributor.departmentDepartment of Immunology, National University Hospital, Reykjavík, Iceland.en
dc.identifier.journalScandinavian journal of immunologyen
html.description.abstractDermatitis herpetiformis (DH), is associated with skin eruptions and granular depositions of IgA in the papillary dermis, but this is not a feature of coeliac disease (CD). The specificity of the IgA in the skin is unknown. High molecular weight glutenin (HMW-g), a component of gluten, has been shown to have structural similarities to human elastin. This paper reports immunoadsorption studies which suggest that human serum may contain antibodies which cross-react with HMW-g and elastin. DH patients had significantly lower levels of IgA antibodies to HMW-g and to elastin than both CD patients and healthy controls. Furthermore, introduction of a gluten-free diet (GFD) was associated with a further reduction in the amount of IgA antibodies to elastin in the DH patients. This diet-associated decrease of elastin antibodies was restricted to the IgA isotype. A significant correlation was observed between IgA antibodies to HMW-g and elastin in healthy controls and CD patients, while no such correlation was found in patients with DH. These findings could indicate that HMW-g induces production of antibodies to elastin, which are deposited in the skin, and that when the antigenic stimulus is removed, these antibodies are further reduced due to continuous dermal deposition. It is postulated that DH may be an autoimmune disease due to cross-reactivity between dietary glutenin and dermal elastin.


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