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Distinct roles for IP-10/C XC L10 in three animal models, Theiler’s virus infection, EA E, and MHV infection, for multiple sclerosis: implication of differing roles for IP-10

Department of Neurology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132-2305, USA

Thomas E Lane

Department of Molecular Biology and Biochemistry, University of California, 3205 Biological Sciences II, Irvine, CA 92697-3900, USA

Jana Blackett

Department of Neurology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132-2305, USA

Robert S Fujinami

Department of Neurology, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132-2305, USA, Robert.Fujinami{at}hsc.utah.edu

Theiler’s murine encephalomyelitis virus (TMEV) causes demyelination with inflammation of the central nervous system (C NS) in mice and is used as an animal model for multiple sclerosis (MS). Interferon-g inducible protein-10 kDa (IP-10) is a C XC chemokine and a chemoattractant for C XC R3⁺ T cells. IP-10 mRNA is expressed in the C NS during TMEV infection. However, administration of anti-IP- 10 serum caused no difference in clinical signs, inflammation, demyelination, virus persistence or anti-virus antibody response in TMEV infection, while levels of virus specific and autoreactive lymphoproliferation increased. This likely reflects a difference in the pathogenesis of TMEV infection from that of two other animal models for MS, mouse hepatitis virus infection and experimental allergic encephalomyelitis (EAE), where blocking of IP-10 resulted in clinical and histological improvement with suppression of antigen specific lymphoproliferation. In this review, we compare and contrast the roles of IP-10 between the three animal models for MS, and discuss the relevance to MS patients with different clinical courses.

Key Words: allergy and immunology • autoimmunity • Cardiovirus infections • histology • immunotherapy • Picornaviridae infections

Multiple Sclerosis, Vol. 10, No. 1, 26-34 (2004)
DOI: 10.1191/1352458504ms982oa


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