Graft rejection syndromes
As the clinical practice of solid organ transplantation evolves in sophistication and frequency, the focus on the mechanisms and subsequent treatment of graft rejection grows. Tissues commonly transplanted include the kidney, liver, heart, lung, and cornea. Bone marrow transplantation is unique in that the host’s immune system is markedly suppressed and an immune-mediated response can occur when cells in the transplanted bone marrow react against host antigens (called graft vs. host disease). The incidence of graft rejection has declined significantly with the improvement in compatibility screening techniques and immunosuppressive regimens.
The donated organ, called an allograft if the donor and recipient are unrelated, is transplanted into the recipient, called the host. Rejection can occur when the host’s immune responses are directed against the graft. The rapidity and reversibility of rejection depend on the various mechanisms involved, such as peritransplant ischemia and mechanical trauma, preformed antibody interactions with graft antigens, alloantigen-reactive T cells, and abnormal tissue remodeling.
Graft rejection syndromes can be divided into three subtypes, based on timing of onset and mechanisms involved.
Hyperacute rejection occurs within minutes to days after graft transplantation. This type of rejection has become rare, affecting less than 1% of transplant recipients because of improved pretransplant screenings. Hyperacute rejection occurs when circulating host antibodies recognize and bind to graft antigens (such as ABO blood group proteins or major histocompatibility complex proteins). Binding of these antibodies leads to initiation of the complement cascade, recruitment of neutrophils, platelet activation, damage to graft endothelial cells, and stimulation of coagulation reactions, which in turn lead to rapid thrombosis, loss of vascular integrity, tissue infarction, and loss of graft function.