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The Journal of Neuroscience, May 10, 2006, 26(19):5143-5152; doi:10.1523/JNEUROSCI.0737-06.2006

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Neurobiology of Disease
Suppressor of Cytokine Signaling 1 Expression Protects Oligodendrocytes from the Deleterious Effects of Interferon-{gamma}

Roumen Balabanov,1,2 Krystal Strand,3,4 April Kemper,5 Ji Yeon Lee,1,2 and Brian Popko1,2

1Jack Miller Center for Peripheral Neuropathy and 2Department of Neurology, The University of Chicago, Chicago, Illinois 60637, 3Neuroscience Center and 4Curriculum for Neurobiology, University of North Carolina, Chapel Hill, North Carolina 27514, and 5Department of Pathology, Wake Forest University Baptist Medical Center, Winston Salem, North Carolina 27157

Correspondence should be addressed to Brian Popko, Jack Miller Center for Peripheral Neuropathy, The University of Chicago, Department of Neurology, 5841 South Maryland Avenue, MC2030, Chicago, IL 60637. Email: bpopko{at}uchicago.edu

Interferon-{gamma} (IFN-{gamma}) is a pleiotropic cytokine produced by T cells and natural killer cells that has been implicated as a deleterious factor in the immune-mediated demyelinating disorder multiple sclerosis. In vitro, purified developing and mature oligodendrocytes have been shown to die in the presence of IFN-{gamma} by apoptosis and necrosis, respectively. Moreover, transgenic expression of IFN-{gamma} in the CNS of mice during development results in tremor, hypomyelination, and oligodendrocyte cell loss, and IFN-{gamma} expression in adult animals after demyelinating insults inhibits remyelination. To examine the molecular mechanisms of IFN-{gamma}-induced oligodendrocyte injury, we generated a transgenic mouse line [PLP/SOCS1 (proteolipid protein/suppressor of cytokine signaling 1)] that exhibits diminished oligodendrocyte responsiveness to IFN-{gamma} attributable to the targeted expression of SOCS1 in these cells. We demonstrate that oligodendrocytes in the PLP/SOCS1 transgenic mice are protected against the injurious effect of IFN-{gamma}. Our data indicate that IFN-{gamma} exerts a direct deleterious effect on developing oligodendrocytes. The capacity of SOCS1 to inhibit the effects of IFN-{gamma} suggests a therapeutic approach toward protection of myelinating oligodendrocytes against the harmful effects of inflammation.

Key words: transgenic mice; SOCS1; interferon-{gamma}; myelin; oligodendrocytes; Stat1

Received Feb. 18, 2006; revised April 3, 2006; accepted April 6, 2006.

Correspondence should be addressed to Brian Popko, Jack Miller Center for Peripheral Neuropathy, The University of Chicago, Department of Neurology, 5841 South Maryland Avenue, MC2030, Chicago, IL 60637. Email: bpopko{at}uchicago.edu




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