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The Journal of Neuroscience, February 21, 2007, 27(8):2013-2024; doi:10.1523/JNEUROSCI.4689-06.2007

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Neurobiology of Disease
Interferon--Oligodendrocyte Interactions in the Regulation of Experimental Autoimmune Encephalomyelitis

Roumen Balabanov,¹ Krystle Strand,³ Rajendra Goswami,² Eileen McMahon,⁴ Wendy Begolka,⁴ Stephen D. Miller,⁴ and Brian Popko¹

¹Jack Miller Center for Peripheral Neuropathy and Department of Neurology and ²Department of Pediatrics, The University of Chicago, Chicago, Illinois 60637, ³Neuroscience Center, The University of North Carolina, Chapel Hill, North Carolina 27514, and ⁴Department of Microbiology-Immunology, Northwestern University, Chicago, Illinois 60611

Correspondence should be addressed to Brian Popko, Jack Miller Center for Peripheral Neuropathy and Department of Neurology, The University of Chicago, MC2030, Room AB 514, 5841 South Maryland Avenue, Chicago, IL 60637. Email: bpopko{at}uchicago.edu

Experimental autoimmune encephalomyelitis (EAE) is an animal model of the human demyelinating disorder multiple sclerosis (MS). The immune cytokine interferon-gamma (IFN-) is believed to participate in disease pathogenesis in both EAE and MS. In the present study, we examined the significance of IFN--oligodendrocyte interactions in the course of EAE. For the purpose of our study, we used the previously described [proteolipid protein/suppressor of cytokine signaling 1 (PLP/SOCS1)] transgenic mouse line that displays suppressed oligodendrocyte responsiveness to IFN-. PLP/SOCS1 mice developed EAE with an accelerated onset associated with enhanced early inflammation and markedly increased oligodendrocyte apoptosis. Moreover, we found that IFN- pretreatment of mature oligodendrocytes in vitro had a protective effect against oxidative stress and the inhibition of proteasome activity and resulted in upregulation in expression of a number of chemokines, including CXCL10 (IP10), CCL2 (MCP-1), CCL3 (MCP-1), and CCL5 (RANTES). These results suggest that IFN--oligodendrocyte interactions are of significance to the clinical and pathological aspects of EAE. In addition, the present study suggests that oligodendrocytes are not simply targets of inflammatory injury but active participants of the neuroimmune network operating during the course of EAE.

Key words: demyelination; oligodendrocytes; inflammation; cytokine; multiple sclerosis; transgenic

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Received Oct. 27, 2006; revised Jan. 7, 2007; accepted Jan. 13, 2007.

Correspondence should be addressed to Brian Popko, Jack Miller Center for Peripheral Neuropathy and Department of Neurology, The University of Chicago, MC2030, Room AB 514, 5841 South Maryland Avenue, Chicago, IL 60637. Email: bpopko{at}uchicago.edu

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