Abstract
T-cell tolerance can be defined as specific unresponsiveness of T cells to a nominal antigen or to an alloantigen. In the case of the nominal antigen, the unresponsiveness is expected to be directed towards peptides derived from the protein and associated with self major histocompatibility complex (MHC) molecules. In the case of the alloantigen, the unresponsiveness is expected to be directed to epitopes on the foreign MHC molecule itself as well as to undefined self-peptides associated with foreign MHC molecules. It is also possible that some peptides derived from foreign MHC molecules could be presented by self MHC molecules (1). Physical elimination of self-reactive T cells during their maturation in the thymus is the best-known mechanism for the establishment of self-tolerance, along with a variety of non-deletional mechanisms of tolerance in the thymus and the periphery (2, 3, 4). A detailed knowledge of tolerance induction in mature peripheral T cells is essential for therapeutic intervention, merely to understand and ensure tolerance in organ transplantation. It must be stressed that 3 different situations might bring about some clue on transplantation tolerance, namely in “in vitro” models, in experimental models and finally in the organ transplant human situation. But this last situation is hardly complex, occuring in an immunological status barely “naïve” and associated with other events which might interfere with the establishment and the maintenance of tolerance such as immunosuppressive drugs, as viral infections, blood transfusions.
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© 1994 Springer Science+Business Media Dordrecht
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Charpentier, B., Alard, P., Hiesse, C., Lantz, O. (1994). Peripheral T Cell Tolerance. In: Touraine, J.L., Traeger, J., Bétuel, H., Dubernard, J.M., Revillard, J.P., Dupuy, C. (eds) Rejection and Tolerance. Transplantation and Clinical Immunology, vol 25. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-0802-7_22
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DOI: https://doi.org/10.1007/978-94-011-0802-7_22
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