STAT4- and STAT6-signaling molecules in a murine model of multiple sclerosis Moses Rodriguez * ,† ,1 , Laurie Zoecklein * , Jeffrey D. Gamez * , Kevin D. Pavelko * , Louisa M. Papke * , Shunya Nakane * , Charles Howe * , Suresh Radhakrishnan † , Michael J. Hansen † , Chella S. David † , Arthur E. Warrington * and Larry R. Pease † Departments of * Neurology and † Immunology, Mayo Clinic, Rochester, Minnesota, USA 1 Correspondence: Department of Neurology, Mayo Clinic, 200 1st Street SW, Rochester, MN 55905, USA. E-mail: rodriguez.moses@mayo.edu <h3>SPECIFIC AIMS</h3> While investigating the CD4 + T cell Th1 (STAT4) and Th2 (STAT6) response to Theiler’s virus infection, we found mice with a demyelinating phenotype that satisfies the requirements for a long incubation period prior to inflammatory demyelination proposed for the human disease multiple sclerosis (MS). Infection of STAT4 –/– mice resulted in a phenotype where prominent inflammatory demyelination similar to MS did not occur until after 180 days after intracerebral infection. <h3>PRINCIPAL FINDINGS</h3> 1. STAT4 –/– but not STAT6 –/– mice developed spinal cord demyelinating lesions very late after virus infection At 45 and 90 days after infection demyelination in
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STAT4- and STAT6-signaling molecules in a murine model of multiple sclerosis
Rodriguez, Moses; Zoecklein, Laurie; Gamez, Jeffrey D.; Pavelko, Kevin D.; Papke, Louisa M.; Nakane, Shunya; Howe, Charles; Radhakrishnan, Suresh; Hansen, Michael J.; David, Chella S.; Warrington, Arthur E.; Pease, Larry R.
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, Volume 20 (2): 343
Fed of American Socs for Experimental Biology – Feb 1, 2006
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