1. Kidney xenotransplantation
Peter J. Cowan, David K.C. Cooper, Anthony J.F. d'Apice 
Kidney International 
Volume 85, Issue 2, Pages (January 2014)
DOI: /ki
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2. Figure 1
Phases of kidney xenograft rejection. (a) Several factors contribute to hyperacute rejection (HAR) of wild-type xenografts, but the key events are the binding of preformed anti-galactose-α1,3-galactose (anti-αGal) antibodies (Abs) to xenograft vascular endothelial cells and subsequent activation of complement. HAR occurs within hours and can be prevented by deletion of αGal (α1,3-galactosyltransferase (GalT) knockout (GTKO)) or transgenic expression of human complement regulatory proteins (hCRPs). (b) Acute humoral rejection of GTKO xenografts is also mediated by antibodies, in this case anti-non-Gal, but is a more prolonged process (days to weeks) that appears to involve the gradual development of a chronic procoagulant and proinflammatory vascular environment.
Kidney International  , DOI: ( /ki )
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3. Figure 2
Donor genetic modification to prevent kidney xenograft rejection. The targets of genetic modification are shown as filled boxes. Ab, antibody; αGal, galactose-α1,3-galactose; CIITA-DN, dominant-negative class II transactivator; CRP, complement regulatory protein; GnT-III, N-acetylglucosaminyltransferase III; GTKO, α1,3-galactosyltransferase knockout; h, human; HLA, human leukocyte antigen; HO1, hemoxygenase-1; HT, H-transferase; Neu5Gc-KO, N-glycolylneuraminic acid knockout; NK cell, natural killer cell; p, pig; shTNFR1, soluble human tumor necrosis factor receptor 1; TFPI, tissue factor pathway inhibitor; Tg, transgenic; TM, thrombomodulin; TRAIL, tumor necrosis factor–related human apoptosis-inducing ligand.
Kidney International  , DOI: ( /ki )
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