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Characterization of the T cell epitopes targeted in MS patients has remained technically challenging, and the functional characteristics of the neuroantigen-specific T cells, particularly in the CNS, have remained unresolved. We have obtained preliminary results showing vigorous T cell responses to MOG peptides in PBL of MS patients by cytokine ELISPOT assay. Based on these results, we want to examine the MOG- specific T cell response in individual patients longitudinally over the course of MS, and test the epitope specificity and functional avidity of these cells.
In support of this, experiments performed during the current funding period have shown that p193 exhibits tumor suppressor activity in NIH-3T3 cells, and that p107 and TSC2 impact upon cardiomyocyte terminal differentiation and proliferation, respectively. In this competitive renewal application, we propose to further test our hypotheses with additional gain and loss of function models. Four Specific Aims are proposed. In Aim number 1, we will generate gain and loss of function transgenic mice to ascertain the role of p193 in normal and pathologic cardiac development, as well as identify the cellular proteins which interact with p193.
Generate_Screen • Project Title: AXONAL PATHOLOGY DURING THE COURSE OF MULTIPLE SCLEROSIS Principal Investigator & Institution: Trapp, Bruce D. Professor; Cleveland Clinic Foundation 9500 Euclid Ave Cleveland, OH 44195 Timing: Fiscal Year 2002 Summary: This proposal is based on the hypothesis that axonal loss is the major cause of irreversible neurological signs and symptoms in multiple sclerosis patients. The principal investigator has designed a series of experiments to address fundamental questions regarding axonal loss and other axonal lesions in multiple sclerosis plaques and in two animal counterparts (Aims 1-3); he also intends in Aim 4 to assess the status of oligodendrocytic precursor cells in and around multiple sclerosis plaques.
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