Due to copyright reasons, an electronic copy of the thesis must be ordered from the faculty. In order for the faculty to have time to process the order, it must be received by the faculty no later than 2 days prior to the public defence. Orders received later than 2 days before the defence will not be processed. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor, Senior Consultant Eystein Sverre Husebye, University of Bergen and Haukeland University Hospital
- Second opponent: Professor Didier Hober, University of Lille, France
- Third member and chair of the evaluation committee: Professor Benedicte A. Lie, University of Oslo
Chair of the Defence
Professor Emerita Trine Bjøro, University of Oslo
Principal Supervisor
Associate Professor, Senior Consultant Sara Salehi Hammerstad, University of Oslo and Oslo University Hospital
Summary
Autoimmune thyroid diseases (AITD), which mainly consist of Graves’ disease and Hashimoto’s thyroiditis, are common and affect quality of life considerably. Yet, no cures exist and the etiology remains elusive. New evidence points to viral infections as possible triggers for autoimmune thyroid disease.
The aims for this doctorate thesis were to explore the viral trigger hypothesis by analyzing antiviral immunoproteins and to confirm the presence of common viruses in thyroid tissue from patients with AITD.
Standard immunohistochemistry and immunofluorescence protocols were applied on formalin-fixed, paraffin-embedded thyroid tissue samples from 118 patients and controls in order to detect HLA class I, STAT 1 and PKR, which are important antiviral proteins and enzymes. Additionally, the enteroviral capsid protein VP1 was assessed. Moreover, we searched for common viruses such as parvovirus B19, human herpesvirus 6, enterovirus, Epstein-Barr virus and cytomegalovirus in snap-frozen thyroid tissue from both AITD patients and controls. For Enterovirus and human herpesvirus 6, we used a novel technique based on pre-enrichment in cell culture, before viral DNA and RNA detection with PCR.
We found significantly more HLA class I in AITD thyroid tissue than in controls. HLA class I and STAT1 were found within the same thyroid cells. Likewise, VP1 was colocalized with PKR, indicating an active antiviral immune response. Enterovirus, as well as human herpesvirus 6 and parvovirus B19, were frequent in thyroid tissue from both patients and controls.
HLA class I upregulation is a defining feature of AITD, which supports the viral trigger hypothesis. Moreover, several common viruses are able to infect the thyroid gland. However, further studies, with additional techniques are needed to verify our findings. Our results may be transferable to other autoimmune diseases, and in its broadest impact might be a step on the way to prevent autoimmune disease.
Additional information
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