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The Journal of Immunology, 2002, 168: 3105-3112.
Copyright © 2002 by The American Association of Immunologists

Increased Severity of Experimental Allergic Encephalomyelitis in lyn-/- Mice in the Absence of Elevated Proinflammatory Cytokine Response in the Central Nervous System

Caigan Du and Subramaniam Sriram1

Department of Neurology, Multiple Sclerosis Research Center, Vanderbilt University Medical Center, Nashville, TN 37212

lyn, a member of the src kinase family, is an important signaling molecule in B cells. lyn-/- mice display hyperactive B-1 cells and IgM hyperglobulinemia. The role of lyn on T cell function and development of Th1-mediated inflammatory disease is not known. Therefore, we examined the effect of disruption of the lyn gene on the development of experimental allergic encephalomyelitis (EAE), a well-established Th1-mediated autoimmune disease. Following immunization with myelin oligodendrocyte protein (MOG) p35-55, lyn-/- mice had higher clinical and pathological severity scores of EAE when compared with wild type (WT). The increase in the severity of EAE in lyn-/- mice was not associated with a commensurate increase in the production of proinflammatory cytokines in the CNS. lyn-/- mice with EAE showed elevation in serum anti-IgM MOG Ab levels over that seen in WT mice, along with a modest increase in the mRNA levels of complement C5 and its receptor, C5aR, in the spinal cord. Transfer of serum from MOG-immunized lyn-/- mice worsened EAE in WT mice, suggesting a pathogenic role for anti-MOG IgM Abs in EAE. These observations underscore the potential role of lyn in regulation of Th1-mediated disease and the role of autoantibodies and complement in the development of EAE.




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