Syngeneic transplants are always accepted; an example is using the patient's own skin to cover a burned area.
Rejection reactions to allogeneic transplants are antigen-specific and produce memory cells
Acute rejection is due to pre-formed antibodies to HLA and other cell-surface antigens such as ABO blood type antigens. Acute rejection begins immediately and kills the donated organ within 30 minutes; it cannot be prevented except by testing recipient serum against donor cells before the transplant.
Chronic rejection is due to T cells recognizing foreign HLA. Chronic rejection takes days to weeks and can usually be controlled with medications that suppress inflammation and T cell activity. Because non-self MHC is similar to self MHC, large numbers of T cells (~5%) can recognize and respond to allogeneic transplants.
Minor histocompatibility antigens are usually non-HLA proteins that differ from one individual to the next; they may also be due to endogenous virus proteins. Rejection due to minor histocompatibility antigens is slower than to MHC proteins.
T cells recognize foreign Class I and Class II MHC on donor APCs and foreign peptides on self APCs.
Activated effector Tc return to the graft and kill the donor cells.
Transplant survivals have improved due to improved tissue typing and improved anti-rejection drugs
Ideally, tissue typing is done both by flow cytometry or cytotoxicity with recipient antibodies and donor cells and by the mixed lymphocyte reaction (MLR). For heart transplants, only blood type antigens are matched due to the short time a heart is viable outside the donor.
In a bone marrow transplant, the immune system of the recipient is destroyed to make room for new donor stem cells. Graft-versus-host disease (GVHD) is caused by mature T cells from the donor rejecting recipient tissues.
Immune suppressants used against transplant rejection include corticosteroids, cyclosporin A and tacrolimus, and antibodies to T cell markers (CD3 and CD2) or antithymocyte serum.
Xenogeneic transplants have been tried in humans but have failed. Work is being done to genetically engineer pigs so that their tissues are antigenically more like human cells. Two approaches are to reduce the expression of cell surface galactose (to which humans have natural antibodies) and to encode expression of complement regulatory proteins DAF and MCP on pig cells.
http://nfs.unipv.it/nfs/minf/dispense/immunology/xenotr.html
Pregnancy is an allogeneic "transplant" situation that is tolerated repeatedly