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Taken together, these studies revealed two important principles: (1) that engineering of human IgG1 for improved binding towards FcRn impairs the pH dependency of its interaction with mouse FcRn, causing increased binding also at pH 7.4 and (2) that increased affinity of the IgG Fc:FcRn interaction at pH 7.4 results in a shortened, not prolonged serum persistence of IgG1 Fc fragments [100]

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