Patrick C. Duncker received his B.S. in Biology, with a minor in Psychology, at the University of California, Irvine in 2009. He joined the Graduate Program in Immunology at the University of Michigan in 2012. In 2013, he joined the laboratory of Dr. Benjamin Segal, and is on track to complete to complete his graduate training in the winter of 2018.
During his undergraduate studies, Patrick’s scientific interests were focused on neuronal damage, protection, and regeneration. In an animal model of Parkinson’s disease, he studied the migration and differentiation of ependymal cells toward exogenous transforming growth factor alpha infused into the striatum. The study sought to show the potential of these cells to function as endogenous adult neural stem cells in the brain. Further, induced migration and differentiation of these cells may provide benefits for diseases marked by neural damage, such as Parkinson’s Disease, Multiple Sclerosis, and Alzheimer’s Disease.
His undergraduate research project aimed to provide neuroprotection again large dose administration of methamphetamine. Binge administration of methamphetamine leads to extensive production of dopamine , glutamate, and serotonin leading to irreversible loss of nerve terminals throughout the striatum and cerebral cortex of the brain. Epidural administration of glutamate receptor antagonists, or administration of dopamine receptor antagonists into the striatum, lead to widespread sparing of dopamine , glutamate, and serotonin synapses throughout the brain.
Upon completion of his undergraduate degree, Patrick worked as a laboratory technician for Dr. Thomas Lane at UC Irvine. Here he was introduced to the interplay of immunology and neuroscience. The projects in which he was engaged utilized a viral-induced model of central nervous system (CNS) demyelination, and sought to understand the immunological mechanisms involved in CNS damage and repair. Using this model, he was involved in demonstrating that Epstein-Barr virus-induced gene 3 negatively regulates viral neuroinflammation by modulating the proinflammatory T cell response to the virus.
Relocating to the University of Michigan for his graduate training, Patrick continued to work within the field of neuroimmunology and joined Dr. Benjamin Segal as a graduate student. Here, he has worked primarily on elucidating the role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in the induction of CNS autoimmune. In this model he demonstrated that, despite the current dogma, GM-CSF is not essential for the development of CNS autoimmunity, but it is required for the long term maintenance of clinical symptoms. Immunological differences observed in the CNS of GM-CSF deficient animals with disease has lead to investigation of new molecular pathways in the model. Particularly, it was observed that the c-c motif cheomkine receptor 1 (CCR1) axis was activated by GM-CSF signalling and appears to promote long term clinical disability. Current research aims to define the role of this GM-CSF:CCR1 pathway in the development of autoimmune demyelination, as well as its connection in other projects within the lab.
- Duncker PC, Stoolman JS, Huber AK, Segal BM (2018). GM-CSF Promotes Chronic Disability in Experimental Autoimmune Encephalomyelitis by Altering the Composition of Central Nervous System-Infiltrating Cells, but Is Dispensable for Disease Induction. J Immunol 200(3):966–973. PMID: 29288202
- Giles DA, Washnock-Schmid JM, Duncker PC, Dahlawi S, Ponath G, Pitt D, Segal BM (2017). Myeloid cell plasticity in the evolution of central nervous system autoimmunity. Ann Neurol. doi:10.1002/ana.25128. PMID: 29283442
- Stoolman JS, Duncker PC, Huber AK, Segal BM (2014). Site-Specific Chemokine Expression Regulates Central Nervous System Inflammation and Determines Clinical Phenotype in Autoimmune Encephalomyelitis. J Immunol 193(2):564–570. PMID: 24928987