T Cell Tolerance and Autoimmunity

  1. Gregory R. Bock Organizer and
  2. Jamie A. Goode
  1. J. F. A. P. Miller1,
  2. W. R. Heath1,
  3. J. Allison1,
  4. G. Morahan1,
  5. M. Hoffmann1,†,
  6. C. Kurts1 and
  7. H. Kosaka2

Published Online: 28 SEP 2007

DOI: 10.1002/9780470515280.ch11

Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms

Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms

How to Cite

Miller, J. F. A. P., Heath, W. R., Allison, J., Morahan, G., Hoffmann, M., Kurts, C. and Kosaka, H. (2007) T Cell Tolerance and Autoimmunity, in Ciba Foundation Symposium 204 - The Molecular Basis of Cellular Defence Mechanisms (eds G. R. Bock and J. A. Goode), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470515280.ch11

Author Information

  1. 1

    The Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia

  2. 2

    Department of Dermatology, Osaka University Medical School, 2–2 Yamada-Oka, Suita, Osaka 565, Japan

  1. Medizinische Hochschule Hannover Klinik fur Abdominal- und Transplantationschirurgie, Postfach 61 01 80, D-3000 Hannover 61, Germany

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471965671

Online ISBN: 9780470515280

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Keywords:

  • T cell tolerance;
  • autoimmunity;
  • autoaggression;
  • autoantigens;
  • T cell receptor

Summary

Many T cells with auto-aggressive potential are deleted in the thymus. Although some of these escape to the general circulation, they do not usually damage organs such as the pancreas. To investigate the mechanisms preventing autoimmunity, we generated transgenic mice expressing known genes under the control of various promoters. We found that the occurrence of autoaggression depended on factors such as the precursor frequency of responding T cells, their state of activation, their accessibility to the autoantigen, the physicochemical properties of the autoantigen, the possibility of priming by environmental antigens which mimic the target antigen, and some inflammatory reaction in the target site.