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Article has an altmetric score of 6

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Referenced in 2 patents
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Research Article Free access | 10.1172/JCI115843

Transplantation of thymic autoimmune microenvironment to severe combined immunodeficiency mice. A new model of myasthenia gravis.

S Schönbeck, F Padberg, R Hohlfeld, and H Wekerle

Max-Planck Institute, Department of Neuroimmunology, Martinsried, Germany.

Find articles by Schönbeck, S. in: JCI | PubMed | Google Scholar

Max-Planck Institute, Department of Neuroimmunology, Martinsried, Germany.

Find articles by Padberg, F. in: JCI | PubMed | Google Scholar

Max-Planck Institute, Department of Neuroimmunology, Martinsried, Germany.

Find articles by Hohlfeld, R. in: JCI | PubMed | Google Scholar

Max-Planck Institute, Department of Neuroimmunology, Martinsried, Germany.

Find articles by Wekerle, H. in: JCI | PubMed | Google Scholar

Published July 1, 1992 - More info

Published in Volume 90, Issue 1 on July 1, 1992
J Clin Invest. 1992;90(1):245–250. https://doi.org/10.1172/JCI115843.
© 1992 The American Society for Clinical Investigation
Published July 1, 1992 - Version history
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Abstract

To study the role of the thymus in the cellular pathogenesis of myasthenia gravis (MG) we transplanted thymus tissue fragments from MG thymuses beneath the kidney capsule of severe combined immunodeficiency (SCID) mice. Immunocytochemical studies documented that the human thymus tissues are accepted as long-term grafts in the host SCID mice, with human lymphocytes, thymic stroma, and thymic myoid cells demonstrable in transplanted thymus for at least 15 weeks after transplantation. Human anti-acetylcholine receptor antibodies became detectable 1 to 2 weeks after transplantation, and in most chimeras the titers increased over at least 11 weeks to reach levels typically found in severe human MG. Human Ig deposits were detected at skeletal muscle end-plates, demonstrating that the human (auto)antibodies bound to murine acetylcholine receptor. In contrast, transfers of dissociated thymus cells only lead to a transient increase of anti-acetylcholine receptor antibodies. Our data prove that myasthenia gravis thymus is able to induce and maintain autoantibody production in immunodeprived host animals, and that this tissue contains all cellular components required for autoantibody production. Transplantation of solid thymus tissue seems to transfer an autoimmune microenvironment, which will allow direct studies of the mechanism of autosensitization inside the thymus.

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Referenced in 2 patents
28 readers on Mendeley
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