Abstract: The invention provides a polypeptide containing at least one IgG Fc region region, said polypeptide having a higher anti-inflammatory activity and a lower cytotoxic activity as compared to an unpurified antibody and methods of production of such polypeptide.

Abstract: Isolated antibodies have been characterized which show specific affinity to a repeating conformational epitope of a protofibril form of the human ?-amyloid peptide as compare to low molecular weight forms of ?-amyloid peptide. These isolated antibodies and related pharmaceutically effective compositions may be useful in the therapeutic and/or prophylactic treatment of Alzheimer's disease by effectively blocking the ability of the protofibril form of ?-amyloid peptide to form fibril forms linked with complications associated with Alzheimer's disease. The isolated antibodies of the present invention are also useful in various diagnostic assays and associated kits.

Abstract: The invention provides a polypeptide containing at least one IgG Fc region, wherein said at least one IgG Fc region is glycosylated with at least one galactose moiety connected to a respective terminal sialic acid moiety by a ? 2, 6 linkage, and wherein said polypeptide having a higher anti-inflammatory activity as compared to an unpurified antibody.

Abstract: A mammalian C-type lectin receptor type is identified which is shown to bind IgG antibodies or Fc fragments, thus inducing IVIG-related reversal of inflammation associated with various immune disorders. The identification of a DC-SIGN receptor type which interacts with IgG to promote a biological response reducing inflammation associated with immune disorders provides for methods of screening and selecting compounds which may be useful in treating various immune disorders by acting to modulate a DC-SIGN(+) cell to signal a second effector macrophage, causing an increase in expression of the Fc?RIIB receptor and in turn inhibiting a cellular-mediated inflammatory response.

Abstract: The present invention is related to enhancing the function of anti-tumor antibodies by regulating Fc?RIIB-mediated activity. In particular disrupting SHIP activation by Fc?RIIB enhances cytotoxicity elicited by a therapeutic antibody in vivo in a human. The invention further provides an antibody, e.g., an anti-tumor antibody, with a variant Fc region that results in binding of the antibody to Fc?RIIB with reduced affinity. A variety of transgenic mouse models demonstrate that the inhibiting Fc?RIIB molecule is a potent regulator of cytotoxicity in vivo.

Abstract: The invention provides methods of altering properties of Fc-containing molecule, comprising altering the sialylation of the oligosaccharides in the Fc region. Proteins having Fc regions having altered sialylation patterns are also provided.

Abstract: The present invention provides reagents, methods and systems for predicting the cytotoxic activity of an antibody or variant thereof comprising: determining a binding affinity of the antibody or variant thereof to a Fc activating receptor; determining a binding affinity of the antibody or variant thereof to a Fc inhibitory receptor, and calculating the ratio of said activating binding affinity to said inhibitory binding affinity (A/I ratio), wherein the magnitude of said ratio is an indication of the cytotoxic activity of the antibody or variant thereof. The present invention also provides purified modified antibodies having altered A/I ratios as compared to the unmodified antibodies.

Abstract: The invention provides a polypeptide containing at least one IgG Fc region, wherein said at least one IgG Fc region is glycosylated with at least one galactose moiety connected to a respective terminal sialic acid moiety by a ?2,6 linkage, and wherein said polypeptide having a higher anti-inflammatory activity as compared to an unpurified antibody.

Abstract: The present invention is related to enhancing the function of anti-tumor antibodies by regulating Fc?RIIB-mediated activity. In particular, disrupting SHIP activation by Fc?RIIB enhances cytotoxicity elicited by a therapeutic antibody in vivo in a human. The invention further provides an antibody, e.g., an anti-tumor antibody, with a variant Fc region that results in binding of the antibody to Fc?RIIB with reduced affinity. A variety of transgenic mouse models demonstrate that the inhibiting Fc?RIIB molecule is a potent regulator of cytotoxicity in vivo.

Abstract: The present invention provides DNA encoding an Fc?RIII(CDl6) receptor protein expressed on NK cells. The invention also provides a stable cell line expressing the Fc?RIII(CDl6) from NK cells. Further provided is a method for determining the presence of HIV-enhancing antibodies and a method for treating an HIV-infected subject.

Abstract: The present invention relates to non-human animals and in vivo methods for testing the efficacy of antibodies directed to antigens expressed by tumors in such animals. In particular, the invention relates to an animal deficient in the expression of one or more Fc receptors. Additionally, such an animal is also immunodeficient, and thus permits the growth of a xenogeneic tumor implant. Such immunodeficient animals may also express human receptors. The present invention also relates to methods of evaluating the enhanced ability of an existing antibody or Fc-modified antibody to act as an immunotherapeutic to eradicate tumor cells or infectious agents.

Abstract: The present invention is related to enhancing the function of anti-tumor antibodies by regulating Fc&ggr;RIIB-mediated activity. In particular, disrupting SHIP activation by Fc&ggr;RIIB enhances cytotoxicity elicited by a therapeutic antibody in vivo in a human. The invention further provides an antibody, e.g., an anti-tumor antibody, with a variant Fc region that results in binding of the antibody to Fc&ggr;RIIB with reduced affinity. A variety of transgenic mouse models demonstrate that the inhibiting Fc&ggr;RIIB molecule is a potent regulator of cytotoxicity in vivo.

Abstract: Disclosed herein is a non-naturally occurring non-human vertebrate animal incapable of expressing a functional Fc receptor which may optionally be capable of expressing a protein which comprises a domain of a human Fc receptor, as well as DNA encoding such Fc receptor-based proteins. Also disclosed are in vivo methods for identifying proinflammatory agents that depend on a functional Fc receptor, in vivo methods for identifying proinflammatory agents that do not depend on a functional Fc receptor, and both in vivo and in vitro methods of identifying anti-inflammatory agents. Pharmaceutical compositions containing, and methods of treating inflammation with anti-inflammatory agents are also described.

Abstract: The present invention provides compositions, methods and kits for the detection of genetic polymorphisms or mutations related to Charcot-Marie-Tooth Disease Type 1B. The polymorphism or mutations generally occur in the protein P0 gene in chromosome 1. Also provided are mutant forms of protein P0 and methods for screening compounds to identify compounds that enhance binding between mutant P0 proteins.

Abstract: This invention provides a method for identifying a cellular protein capable of specifically binding to an activated antibody receptor, whose cytoplasmic domain comprising an ARH1 motif, comprising (a) obtaining cells comprising receptors having the ARH1 motif; (b) lysing the cells under conditions whereby the native complex of the receptor having the ARH1 motif and the cellular protein is preserved;(c) isolating the complex; and (d) testing the associated receptor and the protein for biochemical activities, thereby identifying the cellular protein capable of specifically binding to an activated antibody receptor, whose cytoplasmic domain comprising an ARH1 motif.

Abstract: The present invention provides compositions, methods and kits for the detection of genetic polymorphisms or mutations related to Charcot-Marie-Tooth Disease Type 1B. The polymorphism or mutations generally occur in the protein P0 gene in chromosome 1. Also provided are mutant forms of protein P0 and methods for screening compounds to identify compounds that enhance binding between mutant P0 proteins.

Abstract: A method for obtaining DNA expressing histidine rich protein of various types of Plasmodia is disclosed. The method involves hybridization with the comparable DNA of P. lophurae. The method of particularly well suited for obtaining P. falciparum DNA, whether it is associated with know or knobless phenotype. Additionally, the invention disclosed a safe method for diagnosing P. falciparum infection.