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2015 ; 23
(Pt B
): 211-216
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Immunobiological barriers to xenotransplantation
#MMPMID26159291
Cooper DKC
; Ekser B
; Tector AJ
Int J Surg
2015[Nov]; 23
(Pt B
): 211-216
PMID26159291
show ga
Binding of natural anti-pig antibodies in humans and nonhuman primates to
carbohydrate antigens expressed on the transplanted pig organ, the most important
of which is galactose-?1,3-galactose (Gal), activate the complement cascade,
which results in destruction of the graft within minutes or hours, known as
hyperacute rejection. Even if antibody is removed from the recipient's blood by
plasmapheresis, recovery of antibody is associated with acute humoral xenograft
rejection. If immunosuppressive therapy is inadequate, the development of high
levels of T cell-dependent elicited anti-pig IgG similarly results in graft
destruction, though classical acute cellular rejection is rarely seen. Vascular
endothelial activation by low levels of anti-nonGal antibody, coupled with
dysregulation of the coagulation-anticoagulation systems between pigs and
primates, leads to a thrombotic microangiopathy in the graft that may be
associated with a consumptive coagulopathy in the recipient. The most successful
approach to overcoming these barriers is by genetically-engineering the pig to
provide it with resistance to the human humoral and cellular immune responses and
to correct the coagulation discrepancies between the two species. Organs and
cells from pigs that (i) do not express the important Gal antigen, (ii) express a
human complement-regulatory protein, and (iii) express a human
coagulation-regulatory protein, when combined with an effective immunosuppressive
regimen, have been associated with prolonged pig graft survival in nonhuman
primates.
|Animals
[MESH]
|Animals, Genetically Modified/immunology
[MESH]
|Antibodies/*immunology
[MESH]
|Blood Coagulation
[MESH]
|Graft Rejection/*immunology/prevention & control
[MESH]
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