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Divisions of
* Immunology and Rheumatology and
Bone Marrow Transplantation, Department of Medicine, Stanford University School of Medicine, Stanford, CA 94305; and
Core Research for Engineering, Science, and Technology and Department of Molecular Immunology, Chiba University Graduate School of Medicine, Chiba, Japan
Immune tolerance to organ transplants has been reported in
laboratory animals and in humans after nonmyeloablative conditioning of
the host and infusion of donor bone marrow cells. We examined the
mechanisms of immune tolerance to mouse cardiac allografts in
MHC-mismatched hosts that developed mixed chimerism after
posttransplant conditioning with a 2-wk course of multiple doses of
lymphoid tissue irradiation, depletive anti-T cell Abs, and an
infusion of donor bone marrow cells. When CD1-/- or
J
281-/- hosts with markedly reduced NK T
cells were used instead of wild-type hosts, then the conditioning
regimen failed to induce tolerance to the heart allografts despite the
development of mixed chimerism. Tolerance could be restored to the
CD1-/- hosts by infusing enriched T cells from the bone
marrow of wild-type mice containing CD1-reactive T cells but not from
CD1-/- host-type mice. Tolerance could not be induced in
either IL-4-/- or IL-10-/- hosts given the
regimen despite the development of chimerism and clonal deletion of
host T cells to donor MHC-Ags in the IL-10-/- hosts. We
conclude that immune tolerance to bone marrow transplants involves
clonal deletion, and tolerance to heart allografts in this model also
involves regulatory CD1-reactive NK T cells.
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