Digital Public Defence: Christian Borgen Lindstad
Cand.med. Christian Borgen Lindstad at Institute of Clinical Medicine will be defending the thesis “Experimental mouse studies on gluten-induced autoimmunity in celiac disease” for the degree of PhD (Philosophiae Doctor).
Photo: Audun Forsell Halaas
The public defence will be held as a video conference over Zoom.
The defence will follow regular procedure as far as possible, hence it will be open to the public and the audience can ask ex auditorio questions when invited to do so.
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.
Digital Trial Lecture – time and place
- First opponent: Professor Peter Lane, University of Birmingham, UK
- Second opponent: Associate Professor Katri Lindfors, Tampere University, Finland
- Third member and chair of the evaluation committee: Professor Marit Inngjerdingen, University of Oslo
Chair of the Defence
Professor II Guttorm Haraldsen, University of Oslo
Professor Ludvig M. Sollid, University of Oslo
Celiac disease is a chronic condition where intake of gluten leads to inflammation in the gut. Autoantibodies targeting the enzyme transglutaminase 2 (TG2) is a hallmark feature. Aims of the thesis were to study mechanisms and consequences of gluten-induced anti-TG2 autoimmunity in celiac disease.
It is remarkable that an otherwise harmless food protein (gluten) drives autoimmunity in some individuals. Interactions between TG2-specific B cells and gluten-specific T cells are likely crucial in the pathogenesis.
First, we utilized an advanced mouse model to study basal mechanisms that drive celiac TG2-autoimmunity. Mice harboring disease-relevant genes from celiac patients allowed us to study the roles of TG2-specific B cells and gluten-specific T cells. We found that these cells readily interact and proliferate when stimulated with complexes of gluten and TG2.
Second, we investigated whether TG2-targeting antibodies mediate inflammation in the gut. Typical anti-TG2 antibodies were injected into mice, followed by evaluation for intestinal damage. We found no signs of disease nor intestinal damage, indicating that these antibodies do not have a direct role in the pathogenesis.
Elucidating the mechanisms that activate TG2-specific B cells and gluten-specific T cells could pave the way for novel therapeutic targets in celiac disease. Moreover, knowledge of the mechanisms behind anti-TG2 autoimmunity could have relevance for other autoimmune diseases.
Contact the research support staff.