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  • Title: Presentation of endogenous acetylcholine receptor epitope by an MHC class II-transfected human muscle cell line to a specific CD4+ T cell clone from a myasthenia gravis patient.
    Author: Baggi F, Nicolle M, Vincent A, Matsuo H, Willcox N, Newsom-Davis J.
    Journal: J Neuroimmunol; 1993 Jul; 46(1-2):57-65. PubMed ID: 7689595.
    Abstract:
    Muscle or thymic myoid cells, if induced to express MHC class II in addition to endogenous acetylcholine receptor (AChR), might present epitopes derived from the AChR to specific CD4+ T cells. These T cells could in turn initiate or maintain the anti-AChR response that is responsible for AChR loss in myasthenia gravis (MG). We transfected the AChR+ TE671 (rhabdomyosarcoma) cells with HLA-DR4 and co-cultured them with the DR4-restricted, CD4+ T cell clone (PM-A1; raised from a hyperplastic thymus of an MG patient and previously shown to recognise all forms of the AChR that contain the sequence alpha 144-156). Significant T cell activation, demonstrated both by 3H-thymidine incorporation and by lysis of the TE671 cells, was found in the presence of added alpha 144-156 and, more importantly, in the absence of exogenous antigen. These results show that MHC class II-expressing muscle or other AChR-expressing cells could present endogenous AChR to pathogenic T cells. This process may be important in the aetiology of MG.
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