Mette C.Dekkers


Type 1 diabetes (T1D) is a consequence of the loss of insulin-producing beta cells in the islets of Langerhans, located in the pancreas. The loss of beta cells is caused by an autoimmune response of which the trigger remains uncertain. Recent studies have found that autoantibody-positive, pre-diabetic patients have a smaller pancreas despite normal beta cell mass, indicating that the exocrine pancreas is affected prior to T1D. Together with the observation of cellular stress and "intermediate" cells at the interface of exocrine and endocrine tissue, this suggests that exocrine malfunction may play a role in triggering beta cell stress and T1D onset. In collaboration with the lab of Elizabeth Carroll at TU Delft, we will investigate the relationship between exocrine dysfunction and endocrine beta cell physiology using a zebrafish model.


Curriculum Vitae:

I studied Biomedical Sciences at the University of Leiden. During my bachelor, I went on a Erasmus Exchange and studied Biomedicine for one semester at the Karolinska Institutet in Stockholm. I continued my studies with the research master Biomedical Sciences at the University of Leiden where I focussed on immunology and stem cell biology. I performed my first internship at the Rheumatology department of the LUMC where I worked on the characterization of autoreactive B cells in Systemic Sclerosis. After that, I joined the CCB and Nephrology department of the LUMC for my final internship. During this project I worked on the generation of hypoimmunogenic induced pluripotent stem cells (iPSCs) for transplantation purposes. After obtaining my master degree, I begun my PhD in December 2021 within the type 1 diabetes group of Dr. Zaldumbide at the CCB.


Collaborate with us

Looking for information on one of our topics, a new place to conduct your research or experienced research to join forces with?  Feel free to contact us.!

Read more