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Research Article| Volume 179, ISSUE 1-2, P173-179, October 2006

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Antibody-mediated neuronal cell signaling in behavior and movement disorders

  • Christine A. Kirvan
    Affiliations
    Department of Biological Sciences, California State University, Sacramento, 6000 J Street, Sacramento, CA 95618-6077, USA
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  • Susan E. Swedo
    Affiliations
    Pediatrics and Developmental Neuropsychiatry Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, 35 Convent Dr., BG 35 MSC 3710, Bethesda, MD 20814, USA
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  • Lisa A. Snider
    Affiliations
    Pediatrics and Developmental Neuropsychiatry Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, 35 Convent Dr., BG 35 MSC 3710, Bethesda, MD 20814, USA
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  • Author Footnotes
    1 Financial support: M.W.C holds grants from the National Heart, Lung, and Blood Institute (HL35280 and HL56267) and the Oklahoma Center for the Advancement of Science and Technology.
    Madeleine W. Cunningham
    Correspondence
    Corresponding author. Tel.: +1 405 271 3128; fax: +1 405 271 2217.
    Footnotes
    1 Financial support: M.W.C holds grants from the National Heart, Lung, and Blood Institute (HL35280 and HL56267) and the Oklahoma Center for the Advancement of Science and Technology.
    Affiliations
    Department of Microbiology and Immunology, University of Oklahoma, HSC, 975 N. E. 10th Street, Biomedical Research Center Room 217, Oklahoma City, OK 73104, USA
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  • Author Footnotes
    1 Financial support: M.W.C holds grants from the National Heart, Lung, and Blood Institute (HL35280 and HL56267) and the Oklahoma Center for the Advancement of Science and Technology.

      Abstract

      Behavioral and movement disorders may have antibody responses where mimicry and signal transduction may lead to neuropsychiatric abnormalities. In our study, antibodies in pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS) reacted with the neuronal cell surface and caudate–putamen and induced calcium–calmodulin dependent protein (CaM) kinase II activity in neuronal cells. Depletion of serum IgG abrogated CaM kinase II cell signaling and reactivity of CSF was blocked by streptococcal antigen N-acetyl-beta-d-glucosamine (GlcNAc). Antibodies against GlcNAc in PANDAS sera were inhibited by lysoganglioside GM1. Results suggest that antibodies from an infection may signal neuronal cells in some behavioral and movement disorders.

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