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Julie Rumble, Ph.D.
e-mail address: jrumble@umich.edu

Mentor: Benjamin Segal, M.D.

Techniques Used:

EAE, adoptive transfer, FACS, tissue culture, elispot, in situ hybridization



Research Description:

Experimental autoimmune encephalomyelitis (EAE) has long been used as a model of inflammatory autoimmune disease that can be informative for human autoimmune disorders such as multiple sclerosis. Until recently, EAE was thought to be primarily mediated by Th1-type CD4 T cells, which function through the cytokine interferon gamma (IFN- g ). However, a newer subtype of CD4 T cell, which produces the proinflammatory cytokine IL-17 (Th17 cell), is currently thought to play a role in the pathogenesis of EAE as well. Our lab recently demonstrated that in an adoptive transfer model of EAE, these two subsets of cells can independently induce disease, which manifests the same clinical symptoms but differing histology and treatment responses. In addition, we have found that loss of these important cytokines changes the disease in unexpected ways. Loss of IFN- g results in more severe EAE, while loss of IL-17R does not significantly change the outcome of disease (except in the absence of IFN- g ). We hypothesize that the relative contribution of Th1 and Th17 cells to EAE represents a spectrum of disease that may reflect differences between multiple sclerosis patients. Thus, of great interest are the factors that are mediating disease in the absence of IFN- g or IL-17. IL-1 b has been shown to be important in EAE induction previously, and its newer isoforms play a role in promoting proinflammatory conditions. We are interested in evaluating how IL-1 b and other members of the IL-1 family affect the development of EAE in our model, which dissects the role of Th1 and Th17 cells in EAE pathogenesis.

 

Publications:

Rumble JM, Duckett CS. 2008. Diverse functions within the IAP family. J Cell Sci. 121:3505-7.

Galban S, Hwang C, Rumble JM, Oetjen KA, Wright CW, Boudreault A, Durkin J, Gillard JW, Jaquith JB, Morris SJ, Duckett CS. 2008. Cytoprotective effects of IAPs revealed by a small molecule antagonist. Biochem J.

Rumble JM, Bertrand MJ, Csomos RA, Wright CW, Albert L, Mak TW, Barker PA, Duckett CS. 2008. Apoptotic sensitivity of murine IAP-deficient cells. Biochem J. 415:21-5.

Wright CW, Rumble JM, Duckett CS. 2007. CD30 activates both the canonical and alternative NF-kappaB pathways in anaplastic large cell lymphoma cells. J Biol Chem. 282:10252-62.

Burstein E, Hoberg JE, Wilkinson AS, Rumble JM, Csomos RA, Komarck CM, Maine GN, Wilkinson JC, Mayo MW, Duckett CS. 2005. COMMD proteins, a novel family of structural and functional homologs of MURR1. J Biol Chem. 280:22222-32.

Wilkinson JC, Richter BW, Wilkinson AS, Burstein E, Rumble JM, Balliu B, Duckett CS. 2004. VIAF, a conserved inhibitor of apoptosis (IAP)-interacting factor that modulates caspase activation. J Biol Chem. 279:51091-9.

Brown SW, Meyers RT, Brennan KM, Rumble JM, Narasimhachari N, Perozzi EF, Ryan JJ, Stewart JK, Fischer-Stenger K. 2003. Catecholamines in a macrophage cell line. J Neuroimmunol. 135:47-55.

 

Honors and Awards:

 


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