Immunologic events leading to the acute rejection of a grafted organ follow three sequential stages: 1) recognition of the antigens fully specific expressed by the allograft; 2) proliferation and differentiation of the T lymphocytes; 3) destruction of the graft mediated by various cellular types: sensitized cytotoxic T lymphocytes, lymphokine activated lymphocytes or macrophage cells, and, more hypothetically, by the so-called "killer" cells. The T lymphocytes infiltrating the grafts during rejection include functionally distinct subsets: inducer T cells (CD4+ cells) and suppressor/cytotoxic cells, T cells (CD8+ cells). In reversible acute rejections the role of activated cytotoxic cells (CD3+ CD8+) seems to be predominant. The functional nature of the lymphoblasts infiltrating the allograft is heterogeneous. It includes cell-mediated cytotoxicity, the proliferative response to alloantigens and the production of lymphokines. Finally, the role of the T cell receptor for the recognition of the antigen appears to be essential. The necessity for the immune system to build up a large repertoire of different T receptors is dependent on a mechanism of genetic coding similar to the one used by immunoglobulins. In the near future, one may hope to alter specifically the repertory of the T receptors used by the lymphocytes responsible for rejection. This would represent the dawn of a new era in transplantation immunity with the beginning or specific immunosuppression.