Chronic Graft-Versus-Host Disease

Abstract

Chronic GVHD develops typically more than three months post transplant, and differs from acute GVHD in its distribution of target organs and clinical presentation. Although generally assumed, it has not been conclusively proven, that acute and chronic GVHD have the same immunopathogenesis: namely, the proliferation of mature donor T-cells in response to histocompatibility alloantigens of the host. In long term stable survivors without chronic GVHD this alloim-munity is apparently blocked by specific suppressor cells which usually are not found in patients with chronic GVHD. It has also been postulated that the establishment of tolerance requires a functioning thymus. Since thymus function can be destroyed by acute GVHD, the lack of thymus function may hamper the development of specific suppressor cells capable of mediating stable graft-host-tolerance. The donor-host directed alloagression may be only an initial event leading to autoimmune symptoms, impaired immune reconstitution and infections.