Abstract: The present disclosure relates to antibodies that bind human Dectin-1, multispecific (e.g., bispecific) binding molecules, and methods of use and production related thereto.

Abstract: The present disclosure relates to multispecific (e.g., bispecific) binding proteins that bind human Dectin-1 and human CD20, and methods of use and production related thereto.

Abstract: The present disclosure relates to a method of depleting or reducing the numbers of disease-causing agents including host cells, or host cells products, microbes or their products in a human subject upon administration of molecule that causes targeted phagocytosis and comprises a binding domain that binds a specific phagocytotic receptor, such as Dectin-1, and a binding domain that binds a specific disease-causing agent. In a specific embodiment, a method of the disclosure depletes or reduces the number of disease-causing agents in tissues, blood, or bone marrow by targeted phagocytosis.

Abstract: The present disclosure relates to antibodies that bind to human CD94, as well as methods, uses, polynucleotides, vectors, host cells, and pharmaceutical compositions related thereto. In some embodiments, the antibodies are human or humanized antibodies that bind to human CD94 and do not block binding between CD94 and HLA-E. In some embodiments, the antibodies cross-react with cynomolgus CD94. In some embodiments, the antibodies do not promote internalization of surface-expressed CD94 to the extent of existing antibodies. In some embodiments, the antibodies promote ADCC targeting cells that express human CD94, e.g., on the cell surface.

Abstract: The present disclosure relates to antibodies that bind to human CD94, as well as methods, uses, polynucleotides, vectors, host cells, and pharmaceutical compositions related thereto. In some embodiments, the antibodies are human or humanized antibodies that bind to human CD94 and do not block binding between CD94 and HLA-E. In some embodiments, the antibodies cross-react with cynomolgus CD94. In some embodiments, the antibodies do not promote internalization of surface-expressed CD94 to the extent of existing antibodies. In some embodiments, the antibodies promote ADCC targeting cells that express human CD94, e.g., on the cell surface.

Abstract: The present disclosure relates to antibodies that bind human Dectin-1, multispecific (e.g., bispecific) binding molecules, and methods of use and production related thereto.

Abstract: The present disclosure relates to antibodies that bind human Dectin-1, multispecific (e.g., bispecific) binding molecules, and methods of use and production related thereto.

Abstract: The present disclosure relates to antibodies that bind to human CD94, as well as methods, uses, polynucleotides, vectors, host cells, and pharmaceutical compositions related thereto. In some embodiments, the antibodies are human or humanized antibodies that bind to human CD94 and do not block binding between CD94 and HLA-E. In some embodiments, the antibodies cross-react with cynomolgus CD94. In some embodiments, the antibodies do not promote internalization of surface-expressed CD94 to the extent of existing antibodies. In some embodiments, the antibodies promote ADCC targeting cells that express human CD94, e.g., on the cell surface.

Abstract: The present disclosure relates to methods of treating diseases or disorders associated with LGL and/or NK cells, methods of reducing or depleting LGL and/or NK cells, and methods of inducing ADCC activity using antibodies that bind to a cell surface protein on LGL and/or NK cells and comprise enhanced ADCC activity. The present invention also relates to a method of depleting or reducing the numbers of large granular lymphocytes and natural killer cells in a human subject upon administration of CD94 or CD57 or NKG2A binding molecule that consists of a part that specifically binds to the CD94 or CD57 or NKG2A receptors and an immunoglobulin Fc part. In a specific embodiment, a method of the invention depletes or reduces the number of large granular lymphocytes and natural killer cells in spleen, blood, bone marrow, joints, or other tissues.

Abstract: The present disclosure relates to a method of depleting or reducing the numbers of disease-causing agents including host cells, or host cells products, microbes or their products in a human subject upon administration of molecule that causes targeted phagocytosis and comprises a binding domain that binds a specific phagocytotic receptor, such as Dectin-1, and a binding domain that binds a specific disease-causing agent. In a specific embodiment, a method of the disclosure depletes or reduces the number of disease-causing agents in tissues, blood, or bone marrow by targeted phagocytosis.

Abstract: The present disclosure relates to antibodies that bind human Dectin-1, multispecific (e.g., bispecific) binding molecules, and methods of use and production related thereto.

Abstract: The present disclosure relates to antibodies that bind to human CD94, as well as methods, uses, polynucleotides, vectors, host cells, and pharmaceutical compositions related thereto. In some embodiments, the antibodies are human or humanized antibodies that bind to human CD94 and do not block binding between CD94 and HLA-E. In some embodiments, the antibodies cross-react with cynomolgus CD94. In some embodiments, the antibodies do not promote internalization of surface-expressed CD94 to the extent of existing antibodies. In some embodiments, the antibodies promote ADCC targeting cells that express human CD94, e.g., on the cell surface.