Patrick Duncker graduated in 2009 with a B.S. in Biological Sciences from the University of California, Irvine. After 3 years of working as a laboratory technician in research labs focusing on drug and autoimmune induced damage to the central nervous system he joined the immunology graduate program at UM, where he continues to study CNS autoimmunity through the use of the animal model for Multiple Sclerosis.
Experimental evidence has suggested that Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) is essential for pathogenesis in many models of autoimmunity, including Experimental Autoimmune Encephalomyelitis (EAE), a model of Multiple Sclerosis (MS). Cerebrospinal fluid from MS patients shows elevated levels of GM-CSF compared to healthy controls, and clinical trials of α-GM-CSF are currently underway. Mice lacking GM-CSF (Csf2-/-) are resistant to EAE induced by immunization with Myelin Oligodendrocyte Glycoprotein (MOG35-55). Although adoptively transferred CD4+ T cells from MOG primed Csf2-/- donors migrate to the CNS, they do not induce clinical deficits in recipient mice. These observations have been interpreted as showing that GM-CSF production by CNS infiltrating CD4+ T cells is essential for the development of EAE. However, published experiments did not distinguish between the role of GM-CSF during T cell priming and/ or differentiation in secondary lymphoid tissues versus its role in the CNS during the effector phase. My research is currently focused on characterizing the role of GM-CSF throughout the course of EAE.