In the JDRF Centre of Excellence at UBC we are lucky to work with outstanding trainees. Four of these brilliant minds are helping the admin team organize events, initiate new events relevant to trainees within the JDRF Centre. You can learn more about each of their projects in the section below.
Samantha Mar (Lynn Lab): “I study the development of glucagon-producing pancreatic alpha cells using human embryonic stem cells. Towards this, I developed a reporter human embryonic stem cell line that allows us to see and purify alpha cells for research. We hope to apply our understanding of alpha cells to further improve cell therapies to treat T1D”.
Natalie Nahirney (Johnson Lab): “My research focuses on trying to understand the initiation of T1D from a beta-cell perspective. Paradoxically, I am looking at an early moderation of insulin production in order to help beta-cells avoid both stress and autoimmune killing that contribute to their untimely demise in T1D. I track diabetes development and cellular changes in genetically modified mice. Through this and similar projects, we hope to gain mechanistic insights into T1D onset that can inform genetic screening and therapeutic interventions.
Sonya Mangat (Levings Lab): “My research is focused on engineering immune cell therapies for type 1 diabetes. I’m utilizing cells that naturally regulate the immune system (i.e. regulatory T cells) and genetically editing them to better suppress the negative immune responses seen in both T1D and islet transplantation.”
Lindsay Pallo (Verchere Lab): “My doctoral research aligns with goal 2 and 3 of the UBC JDRF Centre of Excellence. One aspect of my thesis is focused on developing an antigen-specific immunotherapy to prevent the autoimmune processes that lead to beta-cell destruction. I am also developing an assay that can measure circulating levels of a precursor species of a protein released by beta cells – (pro-)islet amyloid polypeptide – from blood of donors living with T1D. These works may lead to a clinical therapy that delays or prevents T1D onset among at-risk individuals, and may enable earlier or more sensitive detection of beta-cell dysfunction, indicating risk for T1D onset, respectively.“
