Pre Existing Recipient Antibodies Mediate Hyperacute Rejection

In rare instances, a transplant is rejected so quickly that the grafted tissue never becomes vascularized. These hyperacute reactions are caused by preexisting host serum antibodies specific for antigens of the graft. The antigen-antibody complexes that form activate the complement system, resulting in an intense infiltration of neutrophils into the grafted tissue. The ensuing inflammatory reaction causes massive blood clots within the capillaries, preventing vascularization of the graft (Figure 21-7).

Pre-existing host antibodies are carried to kidney graft

Antibodies bind to antigens of renal capillaries and activate complement (C-)

Antibodies bind to antigens of renal capillaries and activate complement (C-)

Pre-existing host antibodies are carried to kidney graft

Hyperacute Rejection

Capillary endothelial walls

Capillary endothelial walls

Complement split products attract neutrophils, which release lytic enzymes

Complement split products attract neutrophils, which release lytic enzymes

FIGURE 21-7

Steps in the hyperacute rejection of a kidney graft.

Neutrophil lytic enzymes destroy endothelial cells; platelets adhere to injured tissue, causing vascular blockage

Several mechanisms can account for the presence of preexisting antibodies specific for allogeneic MHC antigens. Recipients of repeated blood transfusions sometimes develop significant levels of antibodies to MHC antigens expressed on white blood cells present in the transfused blood. If some of these MHC antigens are the same as those on a subsequent graft, then the antibodies can react with the graft, inducing a hyperacute rejection reaction. With repeated pregnancies, women are exposed to the paternal alloantigens of the fetus and may develop antibodies to these antigens. Finally, individuals who have had a previous graft sometimes have high levels of antibodies to the allogeneic MHC antigens of that graft.

In some cases, the preexisting antibodies participating in hyperacute graft rejection may be specific for blood-group antigens in the graft. If tissue typing and ABO blood-group typing are performed prior to transplantation, these preexisting antibodies can be detected and grafts that would result in hyperacute rejection can be avoided. Xenotransplants are often rejected in a hyperacute manner because of antibodies to cellular antigens of the donor species that are not present in the recipient species. Such an antigen is discussed in the Clinical Focus section of this chapter.

In addition to the hyperacute rejection mediated by preexisting antibodies, there is a less frequent form of rejection termed accelerated rejection caused by antibodies that are produced immediately after transplantation.

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