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Glycan antigens implicated in hyperacute rejection are cell-surface carbohydrate structures recognized as "non-self" by the recipient’s immune system. Prominent examples include the α1,3-galactose (Gal) antigen in pig xenotransplantation and ABO blood group antigens in humans. Hyperacute rejection occurs when preformed recipient antibodies bind these antigens immediately after transplantation, activating the classical complement pathway and causing rapid, irreversible injury and loss of the graft. Strategies to mitigate this form of rejection include removal of glycan antigens from donor tissues, immunosuppression, and complement inhibition. Glycan antigens represent a major immunological barrier to successful transplantation, necessitating advanced compatibility testing and donor modification.
Drugs and modifications act by reducing antibody binding to glycan antigens, thereby: Preventing complement activation; Reducing inflammatory and cytotoxic immune responses; Minimizing immune-mediated destruction of graft tissue.
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