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Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model.

Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Research Abstract Details 

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  • Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Abstract Text:

    helmar c lehmannHelmar C Lehmann,pablo h h lopezPablo H H Lopez,gang zhangGang Zhang,thien ngyuenThien Ngyuen,jiangyang zhangJiangyang Zhang,bernd c kieseierBernd C Kieseier,susumu moriSusumu Mori,kazim a sheikhKazim A Sheikh,

    Recent studies have proposed that neurite outgrowth is influenced by specific nerve cell surface gangliosides, which are sialic acid-containing glycosphingolipids highly enriched in the mammalian nervous system. For example, the endogenous lectin, myelin-associated glycoprotein (MAG), is reported to bind to axonal gangliosides (GD1a and GT1b) to inhibit neurite outgrowth. Clustering of gangliosides in the absence of inhibitors such as MAG is also shown to inhibit neurite outgrowth in culture. In some human autoimmune PNS and CNS disorders, autoantibodies against GD1a or other gangliosides are implicated in pathophysiology. Because of neurobiological and clinical relevance, we asked whether anti-GD1a antibodies inhibit regeneration of injured axons in vivo. Passive transfer of anti-GD1a antibody severely inhibited axon regeneration after PNS injury in mice. In mutant mice with altered ganglioside or complement expression, inhibition by antibodies was mediated directly through GD1a and was independent of complement-induced cytolytic injury. The impaired regenerative responses and ultrastructure of injured peripheral axons mimicked the abortive regeneration typically seen after CNS injury. These data demonstrate that inhibition of axon regeneration is induced directly by engaging cell surface gangliosides in vivo and imply that circulating autoimmune antibodies can inhibit axon regeneration through neuronal gangliosides independent of endogenous regeneration inhibitors such as MAG.

    Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Publishing Authors By Initials

    hc lehmannHC Lehmann,ph lopezPH Lopez,g zhangG Zhang,t ngyuenT Ngyuen,j zhangJ Zhang,bc kieseierBC Kieseier,s moriS Mori,ka sheikhKA Sheikh,

    For similar diagnosis: prognosis: treatment outcome research abstracts see: diagnosis: prognosis: treatment outcome research

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    Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of neuroscience : the official journal

    VOLUME: 27

    Page Numbers: 27-34

    Journal Abbreviation: J. Neurosci.

    ISSN: 1529-2401

    DAY: 3

    MONTH: Jan

    YEAR: 2007

    Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8102140

    Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Keywords Mesh Terms:

    KEYWORDS: Treatment Outcome

    MESH TERMS: prevention & control

    Chemical & Substance for Abstract: Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model. Information

    Substance Name: ganglioside, GD1a

    Registry Number: 12707-58-3

    Grant and Affiliation Information for Passive immunization with anti-ganglioside antibodies directly inhibits axon regeneration in an animal model.

    AFFILIATION: Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NINDS

    GRANT: NS42888

    ACRONYM: NS

    MEDLINETA: J Neurosci

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    ACCESSION NUMBER:

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