Transplant rejection can be classified as hyperacute, acute, or chronic. Hyperacute rejection is usually caused by specific antibodies against the graft and occurs within minutes or hours after grafting.
Chronic rejection is the leading cause of organ transplant failure. The organ slowly loses its function and symptoms start to appear. This type of rejection cannot be effectively treated with medicines.
Transplant rejection can be classified into three types: hyperacute, acute, and chronic. These types are differentiated by how quickly the recipient's immune system is activated and the specific aspect or aspects of immunity involved.
The process of graft rejection can be divided into two phases: (1) a sensitization phase in which antigen reactive lymphocytes in the recipient's lymph node proliferate in response to the donor's alloantigens and (2) an effector phase in which the recipient's sensitized effector cells mediate immune destruction of the ...
Hyperacute rejection is caused by the presence of antidonor antibodies existing in the recipient before transplantation. These antibodies induce both complement activation and stimulation of endothelial cells to secrete Von Willebrand procoagulant factor, resulting in platelet adhesion and aggregation.
Hyperacute rejection is usually caused by specific antibodies against the graft and occurs within minutes or hours after grafting. Acute rejection occurs days or weeks after transplantation and can be caused by specific lymphocytes in the recipient that recognize human leukocyte antigens in the tissue or organ grafted.
In general, when transplanting tissue or cells from a genetically different donor to the graft recipient, the alloantigen of the donor induces an immune response in the recipient against the graft. This response can destroy the graft if not controlled. The whole process is called allograft rejection.
Acute rejection
Acute cellular rejection is mediated by lymphocytes that have been activated against donor antigens, primarily in the lymphoid tissues of the recipient. The donor dendritic cells (also called passenger leukocytes) enter the circulation and function as antigen-presenting cells (APCs).
Acute rejection happens when your body's immune system treats the new organ like a foreign object and attacks it. We treat this by reducing your immune system's response with medication. Chronic rejection can become a long-term problem.
Depending on the timing of their development, the rejection has been classified in hyperacute, acute, and chronic. 7 This article will explore the immune response behind organ rejection; besides, the emphasis will be placed on some details of this rejection.
Acute rejection can occur at any time, but it is most common from one week to three months after transplant surgery. Fifteen percent or less of patients who receive a deceased donor kidney transplant will have an episode of acute rejection.
Acute transplant rejection occurs days to months after a transplant when the immune system identifies a grafted organ as foreign and attacks it. Acute transplant rejection is common and the prognosis is guarded.
In most experimental transplant models, kidney and liver allografts evoke a weaker rejection response than heart and lung allografts. Moreover, kidney and liver allografts can actively participate in the induction and maintenance of tolerance and thus, can be considered “tolerance-prone” organs.
Most rejections are mild and easily treated by making adjustments to immunosuppression medication dosages. Rejection occurs most often in the first six months after transplant.
To reduce the chances of transplant rejection and loss of a transplant, the following steps are taken before transplantation occurs: Ensure recipient and donor have compatible blood types. Perform genetic testing to ensure compatible recipient and donor matches.
In heart transplants, the rate of organ rejection and patient mortality are the highest, even though the transplants are monitored by regular biopsies. Specifically, some 40% of heart recipients experience some type of severe rejection within one year of their transplant.
Acute rejection can occur in the first few months (particularly the first few weeks) after a transplant. It is common - about 15% of people experience acute rejection in the first three months after a transplant.
Tissue biopsy remains the gold standard for evaluating immunologic graft damage, and the histologic definition of acute rejection has evolved in recent years. Intravenous steroids and T cell depletion remain the standard therapy for T cell–mediated rejection and are effective in reversing most cases.
Most rejection episodes can be reversed if detected and treated early. Treatment for rejection is determined by severity. The treatment may include giving you high doses of intravenous steroids called Solumedrol, changing the dosages of your anti-rejection medications, or adding new medications.
Usually, high dose steroids and basal immunosuppression optimization are the first line of therapy in treating acute cellular rejection.
Acute renal allograft rejection is a major cause of allograft dysfunction. Some kidneys do not regain function even with maximal antirejection therapy. Even among patients who recover, acute rejection episodes can have a negative impact on long-term graft survival.
The most common type of heart transplant rejection is called acute cellular rejection. This happens when your T-cells (part of your immune system) attack the cells of your new heart. It happens most often in the first 3 to 6 months after transplant.
However, when skin is grafted between unrelated or allogeneic individuals (an allograft), the graft is initially accepted but is then rejected about 10–13 days after grafting (Fig. 13.22). This response is called a first-set rejection and is quite consistent.
Cellular Xenograft Rejection. Unlike HAR and AHXR, cellular xenograft rejection is relevant to both whole organ grafts and cellular grafts. It results in rejection that may occur days to weeks after transplantation (37). Cellular rejection of a xenograft can be mediated by innate and adaptive immune responses.
Humoral rejection is mediated by T-cell stimulation of endothelial cells and is associated with allosensitization by a previous transplant, transfusion, pregnancy, or ventricular assist device use. The incidence varies from center to center, and the diagnostic criteria are controversial.