Research Article| Volume 306, ISSUE 1-2, P9-15, July 15, 2011

Accelerated central nervous system autoimmunity in BAFF-receptor-deficient mice

  • Susan S. Kim
    Correspondence to: S. Kim, 1515 Newton Court, Room 510, Davis, CA 95618, United States. Tel.: +1 530 754 5013; fax: +1 530 754 5036.
    Department of Neurology and Neuroscience Graduate Program, University of California Davis, Davis, CA, United States
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  • David P. Richman
    Department of Neurology and Neuroscience Graduate Program, University of California Davis, Davis, CA, United States
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  • Scott S. Zamvil
    Correspondence to: S. Zamvil, Department of Neurology, University of California, San Francisco, 513 Parnassus Avenue, S-268, San Francisco, CA 94143, United States. Tel.: +1 415 502 7395; fax: +1 415 502 8512.
    Department of Neurology and Program in Immunology, University of California, San Francisco, San Francisco, CA, United States
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  • Mark A. Agius
    Department of Neurology and Neuroscience Graduate Program, University of California Davis, Davis, CA, United States

    Veterans Administration Northern California Health Care System, Mather, CA, United States
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Published:April 29, 2011DOI:


      B cell activating factor (BAFF) is critical for B cell survival, a function that is mediated by BAFF receptor, (BAFF-R). The role of BAFF (or BAFF-R) in the multiple sclerosis model, experimental autoimmune encephalomyelitis (EAE), was examined using BAFF-R-deficient mice. BAFF-R deficiency resulted in paradoxically increased severity of EAE induced by myelin-oligodendrocyte glycoprotein (MOG) peptide 35–55. Inflammatory foci in BAFF-R-deficient mice comprised increased numbers of activated macrophages expressing BAFF and correlated with increased BAFF secretion. Thus, BAFF-R may be important in EAE pathogenesis, possibly by influencing macrophage function through a mechanism that involves modulation of BAFF expression.


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