The immune system in humans and monkeys responds vigorously against α‐gal (α‐galactosyl, Galα1‐3Galβ1‐4GIcNAc‐R) epitopes on xenografts by producing large amounts of high‐affinity anti‐Gal immunoglobulin G molecules. These antibody molecules may exacerbate chronic rejection of xenografts via several mechanisms including: antibody‐dependent cell cytotoxicity, chronic activation of endothelial cells, and increasing immunogenicity of xenograft‐specific antigens by targeting them to antigen‐presenting cells.
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Galili et al. (1997) studied this question.
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