General principles

In recent years, major advances have been made in understanding the immunological mechanisms involved in immune nonreactivity to self, i.e. self-tolerance. Three broad mechanisms to prevent the action of potentially antiself-reactive lymphocyte clones appear possible: destruction (clonal deletion); continued survival but nonreactivity (clonal anergy); and suppression by regulatory T cells (clonal suppression). How these mechanisms relate to those involved in nonreactivity to grafted tissue is not certain. Where hematopoietic chimerism is induced, allowing bone marrow stem cells of donor type to seed the recipient thymus, the mechanisms of non-reactivity might be similar to those of self-tolerance.

However, in most clinically relevant situations, involving adult recipients of solid organ grafts, the predominant mechanism is likely to be that of T cell-mediated suppression.

A variety of additional factors, not applicable in self-tolerance, might also be operating in adult transplant recipients, e.g. altered immunogenicity of the graft, antibody-mediated suppression.

Traditionally, there have been two major approaches to donor-specific immunosuppression in transplantation:

1. Antigen-induced suppression (active enhancement) refers to specific immunosuppression induced by treatment of the recipient with preparations containing donor histocompatibility antigens.

2. Antibody-induced suppression (passive enhancement) refers to specific immunosuppression induced by treatment of the recipient with antibodies directed at donor histocompatibility antigens.

Over the past few years, there has been renewed interest in the potential of anti-idiotypic immunity for regulating immune responses. Very impressive work has been done on the suppression of experimental autoimmune encephalomyelitis (EAE) by immunizing with autologous T cell clones and even synthetic peptides corresponding to T cell receptor variable regions. However, whether or not these ideas can be translated in practice to the more complex area of immunosuppression in clinical transplantation remains to be seen.

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