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Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue.

Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Research Abstract Details 

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  • Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Abstract Text:

    f shawn galinF Shawn Galin,cheryl l chrismanCheryl L Chrisman,james r cookJames R Cook,likang xuLikang Xu,patricia l jacksonPatricia L Jackson,brett d noeragerBrett D Noerager,nathaniel m weathingtonNathaniel M Weathington,j edwin blalockJ Edwin Blalock,

    Myasthenia gravis (MG) is caused by T cell-dependent antibodies reactive with acetylcholine receptors. These autoreactive antibodies cause muscle weakness by interfering with neuromuscular transmission via removal of acetylcholine receptors from the neuromuscular junction as well as changing the architecture of the junction itself. Consequently, muscle fatigue is a debilitating aspect of MG often leading to more general feelings of tiredness not directly due to muscle weakness. We have previously described two peptides that are mimetics of antigen receptors on certain autoreactive T and B cells that are involved in MG. When used as vaccines in the rat model of MG, these peptides prevented and ameliorated disease and muscle fatigue by blunting acetylcholine receptor antibody responses. Such disease protection resulted from vaccine-induced anergizing antibodies against acetylcholine receptor-specific T and B cell antigen receptors. The present study prospectively evaluated the efficacy of these two vaccines in spontaneous acquired MG in pet dogs. When compared to historical controls that were prospectively studied, the vaccines increased the proportion of remitted dogs from 17 to 75%. In comparison to retrospectively studied historical controls that spontaneously remitted from MG, the vaccines accelerated the rate of decline in acetylcholine receptor antibody titers which resulted in a 3-fold decrease in the mean time to remission. These results are suggestive of a new type of targeted therapy that can drive autoimmune responses into long-term remission and possibly afford a means of determining whether correction of a physical cause of muscle weakness also corrects the perception of chronic, generalized fatigue.

    Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Publishing Authors By Initials

    fs galinFS Galin,cl chrismanCL Chrisman,jr cookJR Cook,l xuL Xu,pl jacksonPL Jackson,bd noeragerBD Noerager,nm weathingtonNM Weathington,je blalockJE Blalock,

    For similar complex mixtures: biological products: vaccines research abstracts see: complex mixtures: biological products: vaccines research

    PUBMED ID PMID:

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    Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Journal Published:

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

    Journal: Brain, behavior, and immunity

    VOLUME: 21

    Page Numbers: 323-31

    Journal Abbreviation: Brain Behav. Immun.

    ISSN: 0889-1591

    DAY: 20

    MONTH: 11

    YEAR: 2006

    Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8800478

    Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Keywords Mesh Terms:

    KEYWORDS: Vaccines

    MESH TERMS: therapeutic use

    Chemical & Substance for Abstract: Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue. Information

    Substance Name: Vaccines

    Registry Number: 0

    Grant and Affiliation Information for Possible therapeutic vaccines for canine myasthenia gravis: implications for the human disease and associated fatigue.

    AFFILIATION: Department of Physiology and Biophysics, University of Alabama at Birmingham, 1918 University Blvd., MCLM 896, Birmingham, AL 35294-0005, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: T32HL007553

    ACRONYM: HL

    MEDLINETA: Brain Behav Immun

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