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The anti-rheumatoid drug D-penicillamine (D-pen) has a reactive sulfhydryl group capable of modifying self antigens, and can provoke typical autoantibody-mediated myasthenia gravis (MG), especially in DR1+ individuals. We have selected T cell clones from one such patient that were highly specific for D-pen but not its L-isomer or D-cysteine. Moreover, they were restricted to HLA-DR1, had a Th1 phenotype and used TCR V alpha4.1, V beta6.1. They responded well to blood mononuclear cells prepulsed with D-pen either in the absence of serum or after chloroquine treatment, but not to autologous D-pen-pulsed B cell lines. Thus, D-pen may directly couple to distinctive peptides resident in surface DR1 molecules on circulating macrophages or dendritic cells.

Original publication




Journal article


Journal of neuroimmunology

Publication Date





146 - 153


Neurosciences Group, Institute of Molecular Medicine, The John Radcliffe Hospital, Headington, Oxford, UK.


CD4-Positive T-Lymphocytes, Cell Line, Humans, Myasthenia Gravis, Autoimmune Diseases, Drug Hypersensitivity, Tritium, Chloroquine, Penicillamine, Blood Proteins, Receptors, Antigen, T-Cell, alpha-beta, Thymidine, Antirheumatic Agents, Histocompatibility Antigens Class II, HLA-DR1 Antigen, Epitopes, Amino Acid Sequence, Base Sequence, Protein Binding, Molecular Sequence Data, Aged, Female, CD3 Complex