Pathology

In mice, thymectomized as young adults, neonatally induced tolerance persists in the putative absence of cell chimerism. The finding provides evidence that a selective deficiency of specific clones of lymphocytes exists in transplantation tolerance when induced under the conditions of these experiments.

Recovery from adoptively terminated transplantation tolerance was studied by utilizing formerly tolerant rats as donors of lymphocytes in local renal graft-vs.-host reactions (GVHR). The origin of the proliferating lymphocytes in the GVHR was studied by means of sex chromosome markers. A deficit of specifically reactive lymphocytes, while tolerance was in effect, was revealed by the continuing absence of autochthonous specifically reactive cells after tolerance was abolished in adult thymectomized chimeras. The findings are consistent with Burnet's hypothesis of the cellular basis of tolerance, but apply only to the T lymphocytes of donor origin which normally proliferate in these GVHR.