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Each individual carries a unique set of polymorphic residues on HLA molecules as well as other endothelial antigens (e.g., non‐synonymous single‐nucleotide polymorphisms in transmembrane proteins, loss of function variants) representing B cell epitopes. Each donor–recipient pair is mismatched for different epitopes. A quantitative approach suggests that a higher number of mismatches predispose for alloantibody development.
