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Benjamin Segal, MD
Granulocyte-Macrophage Colony-Stimulating Factor: Dual Roles in Autoimmune Encephalomyelitis
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.
Stoolman JS, Duncker PC, Huber AK, Segal BM. Site-specific chemokine expression regulates central nervous system inflammation and determines clinical phenotype in autoimmune encephalomyelitis. J Immunol. 2014 Jul 15;193(2):564-70. doi: 10.4049/jimmunol.1400825. Epub 2014 Jun 13.