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Autoantibodies to α-fodrin in primary Sjögren's syndrome and SLE detected by an in vitro transcription and translation assay
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Sciences.
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2003 In: Clinical and Experimental Rheumatology, Vol. 21, 49-56 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2003. Vol. 21, 49-56 p.
URN: urn:nbn:se:uu:diva-93508OAI: oai:DiVA.org:uu-93508DiVA: diva2:167003
Available from: 2005-10-05 Created: 2005-10-05Bibliographically approved
In thesis
1. Clinical and Experimental Studies in Primary Sjögren’s Syndrome and Systemic Lupus Erythematosus
Open this publication in new window or tab >>Clinical and Experimental Studies in Primary Sjögren’s Syndrome and Systemic Lupus Erythematosus
2005 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Autoimmune mechanisms and genetic susceptibility contribute to the pathogenesis of primary Sjögren’s syndrome and SLE. These chronic systemic autoimmune diseases have many serological and clinical features in common and have an impact on daily life. The studies in this thesis aim to elucidate their autoimmune mechanisms, define susceptibility genes and evaluate effects of androgen supplement on health-related quality of life.

Autoantibodies against α-fodrin, a widely distributed cytoskeletal protein, were detected at similar frequencies in sera from patients with primary and secondary Sjögren’s syndrome and SLE. Consequently, testing for antibodies against α-fodrin would not add diagnostic value compared to conventional serological analysis and does not discriminate between these diseases.

The type I interferon (IFN) system was found to be activated in primary Sjögren’s syndrome. IFN-α containing cells were detected in minor salivary gland biopsies, while sera from patients with primary Sjögren’s syndrome induced IFN-α production in the presence of apoptotic and necrotic cell material. This ability of sera correlated with the presence of antibodies against RNA-binding proteins and IFN-α production was dependent on RNA in immune complexes. The natural interferon producing cells/plasmacytoid dendritic cells (NIPC/PDC) were the IFN-α producers and blocking of FcγRIIa inhibited the production. Single nucleotide polymorphisms (SNPs) in two genes in the type I IFN signalling pathway, those for tyrosine kinase 2 and interferon regulatory factor 5, were strongly associated with SLE in a Swedish, Finnish and Icelandic population. The minor allele frequencies were lower in SLE patients than in healthy controls. These SNPs may decrease the function of the type I IFN system, thereby conferring protection against SLE.

Supplementation with dehydroepiandrosterone (DHEA) in glucocorticoid treated women with SLE led to mild improvements in health-related quality of life in respect of mental well-being and sexuality, whereas physical well-being was unaffected.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2005. 76 p.
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 73
Medicine, Sjögren’s syndrome, SLE, α-fodrin, interferon-α, single nucleotide polymorphism, dehydroepiandrosterone, Medicin
National Category
Dermatology and Venereal Diseases
urn:nbn:se:uu:diva-5943 (URN)91-554-6349-5 (ISBN)
Public defence
2005-10-28, Rudbecksalen, Rudbecklaboratoriet, Uppsala, 13:15
Available from: 2005-10-05 Created: 2005-10-05 Last updated: 2012-03-30Bibliographically approved

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