<unk> D pathology Three criteria, known as the Billingham criteria, must be met in order for<unk> D to occur. * An immuno-competent graft is administered, with viable and functional immune cells. * The recipient is immunologically different from the donor – histo-incompatible. * The recipient is immunocompromised and therefore cannot destroy or inactivate the transplanted cells. After bone marrow transplantation, T cells present in the graft, either as contaminants or intentionally introduced into the<unk> , attack the tissues of the transplant recipient after perceiving<unk>  tissues as antigenically foreign. The T cells produce an excess of cytokines, including TNF-α and interferon-gamma (IFNγ). A wide range of<unk>  antigens can initiate<unk> , among them the human leukocyte antigens (HLA). However,<unk>  can occur even when HLA-identical siblings are the donors. HLA-identical siblings or HLA-identical unrelated donors often have genetically different proteins (called minor histocompatibility antigens) that can be presented by major histocompatibility complex (MHC) molecules to the donor's T-cells, which see these antigens as foreign and so mount an immune response. Antigens most responsible for graft loss are HLA-DR (first six months), HLA-B (first two years), and HLA-A (long-term survival). While donor T-cells are undesirable as effector cells of<unk> , they are valuable for engraftment by preventing the recipient's residual immune system from rejecting the bone marrow graft <unk> -versus-graft). In addition, as bone marrow transplantation is frequently used to treat cancer, mainly leukemias, donor T-cells have proven to have a valuable graft-versus-tumor effect. A great deal of current research on allogeneic bone marrow transplantation involves attempts to separate the undesirable graft-vs-host disease aspects of T-cell physiology from the desirable graft-versus-tumor effect. Transfusion-associated<unk> D This type of<unk> D is associated with transfusion of un-irradiated blood to immunocompromised recipients. It can also occur in situations in which the blood donor is homozygous and the recipient is heterozygous for an HLA haplotype. It is associated with higher mortality (80–90%) due to involvement of bone marrow lymphoid tissue, however the clinical manifestations are similar to<unk> D resulting from bone marrow transplantation. Transfusion-associated<unk> D is rare in modern medicine. It is almost entirely preventable by controlled irradiation of blood products to inactivate the white blood cells (including lymphocytes) within. Thymus transplantation Thymus transplantation may be said to be able to cause a special type of<unk> D because the recipient's thymocytes would use the donor thymus cells as models when going through the negative selection to recognize self-antigens, and could therefore still mistake own structures in the rest of the body for being non-self. This is a rather indirect<unk> D because it is not directly cells in the graft itself that causes it but cells in the graft that make the recipient's T cells act like donor T cells. It can be seen as a multiple-organ autoimmunity in xenotransplantation experiments of the thymus between different species. Autoimmune disease is a frequent complication after human allogeneic thymus transplantation, found in 42% of subjects over 1 year post transplantation. However, this is partially explained by the fact that the indication itself, that is, complete DiGeorge syndrome, increases the risk of autoimmune disease. Thymoma-associated multiorgan autoimmunity (TAMA) A<unk> D-like disease called thymoma-associated multiorgan autoimmunity (TAMA) can occur in patients with thymoma. In these patients rather than a donor being a source of pathogenic T cells, the patient's own malignant thymus produces self-directed T cells. This is because the malignant thymus is incapable of appropriately educating developing thymocytes to eliminate self-reactive T cells. The end result is a disease virtually indistinguishable from<unk> D.
Graft-versus-host disease
Transplant rejection
Cardiac allograft vasculopathy
Vasculogenic mimicry
Infectious tolerance
Disseminated disease
Chronic allograft nephropathy
Post-transplant lymphoproliferative disorder