Abstract
Graft-versus-host disease (GVHD) develops when donor T cells recognize host alloantigens expressed on host-derived antigen presenting cells. Langerhans cells and donor-derived antigen presenting cells are also involved in the development of GVHD. Innate immunity can potentiate antigen-specific donor T cell responses toward host alloantigens. Effectors of acute GVHD include both cytotoxic T lymphocytes and inflammatory cytokines. Alloantigen expression on host target epithelium is not always necessary to induce acute GVHD, augments acute GVHD, and may suppress graft-versus-leukemia (GVL) effects. Impaired thymic function may be involved in the development of chronic GVHD.
