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AssigneeMiltenyi Biotec GmbH
InventorsIris Bürger, Martin Meyer, Andrzej Dzionek
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The present invention relates to polypeptides comprising a mutant human IgG4, which mutant human IgG4 is capable of increasing the binding to and activation of immunoreceptor tyrosine-based inhibitory motif (ITIM)-containing FcγRIIb/c (CD32b), but not FcγRIIa (CD32a). More specifically, the invention relates to polypeptides comprising at least one human IgG4 with a lysine at position 409 (409K), using the EU index according to Kabat et al., which IgG4 is capable of binding to human CD32b/c with a statistically significant (p=0.05) higher binding affinity than a wild-type human IgG1 and than a wild-type human IgG4, for use in the prevention and/or treatment of an autoimmune disease or allergy, as further defined in the claims.
A method of activating human CD32b/c on CD32b/c expressing cells in the treatment of an autoimmune disease in a human subject, comprising the step of administering to said human subject a polypeptide comprising at least one human IgG4 with a lysine at position 409 (409K), using the EU index according to Kabat, wherein the IgG4 recognizes an epitope of BDCA-2 (CD303) and is capable of binding to human CD32b/c with a statistically significant (p=0.05) higher binding affinity than a wild-type human IgG1 having the amino acid sequence of SEQ ID NO:
A method of activating human CD32b/c on CD32b/c expressing cells in the treatment of allergy in a human subject, comprising the step of administering to said human subject a polypeptide comprising at least one human IgG4 with a lysine at position 409 (409K), using the EU index according to Kabat, wherein the IgG4 recognizes an epitope of BDCA-2 (CD303) and is capable of binding to human CD32b/c with a statistically significant (p=0.05) higher binding affinity than a wild-type human IgG1 having the amino acid sequence of SEQ ID NO:
Dependencies are inferred from the claim text.