Patent classifications
C07K16/16
Anti-gliadin antibodies, encoding nucleic acids and methods of detecting gliadin
The present invention provides anti-gliadin antibodies and antibody fragments, and polypeptides encoding the antibodies or fragment. Also disclosed are methods and Kits for the use of such antibodies, fragments, or polypeptides in detection of gliadin. Further provided are heavy chain and light chain variable sequences and associated sequences of complementarity-determining regions (CDRs).
Anti-gliadin antibodies, encoding nucleic acids and methods of detecting gliadin
The present invention provides anti-gliadin antibodies and antibody fragments, and polypeptides encoding the antibodies or fragment. Also disclosed are methods and Kits for the use of such antibodies, fragments, or polypeptides in detection of gliadin. Further provided are heavy chain and light chain variable sequences and associated sequences of complementarity-determining regions (CDRs).
BRASSICA GAT EVENT AND COMPOSITIONS AND METHODS FOR THE IDENTIFICATION AND/OR DETECTION THEREOF
Compositions and methods related to transgenic glyphosate tolerant Brassica plants are provided. Specifically, the present invention provides Brassica plants having a DP-073496-4 event which imparts tolerance to glyphosate. The Brassica plant harboring the DP-073496-4 event at the recited chromosomal location comprises genomic/transgene junctions within SEQ ID NO: 2 or with genomic/transgene junctions as set forth in SEQ ID NO: 12 and/or 13. The characterization of the genomic insertion site of the event provides for an enhanced breeding efficiency and enables the use of molecular markers to track the transgene insert in the breeding populations and progeny thereof. Various methods and compositions for the identification, detection, and use of the event are provided.
BRASSICA GAT EVENT AND COMPOSITIONS AND METHODS FOR THE IDENTIFICATION AND/OR DETECTION THEREOF
Compositions and methods related to transgenic glyphosate tolerant Brassica plants are provided. Specifically, the present invention provides Brassica plants having a DP-073496-4 event which imparts tolerance to glyphosate. The Brassica plant harboring the DP-073496-4 event at the recited chromosomal location comprises genomic/transgene junctions within SEQ ID NO: 2 or with genomic/transgene junctions as set forth in SEQ ID NO: 12 and/or 13. The characterization of the genomic insertion site of the event provides for an enhanced breeding efficiency and enables the use of molecular markers to track the transgene insert in the breeding populations and progeny thereof. Various methods and compositions for the identification, detection, and use of the event are provided.
CHIMERIC ANTIGEN RECEPTOR TO WHICH ANTI-COTININE ANTIBODY IS LINKED, AND USE THEREOF
A chimeric antibody receptors with anti-cotinine antibodies linked, and uses thereof are disclosed. A T cell presenting the chimeric antibody receptor on the surface secretes interferon gamma specifically for a target molecule of a cotinine-conjugated binding molecule that is added together therewith and induces cell death of the cell expressing the target molecule by the T cell. On the contrary, by administering a cytotoxic agent conjugated with cotinine, cell death of the chimeric antigen receptor T cell is induced. Therefore, if necessary, a cytotoxic agent conjugated with cotinine can be administered to remove the chimeric antigen receptor T cells that have been already administered, thereby suppressing immune side effects due to hyperactivity of T cells. Thus, the chimeric antigen receptor to which the anti-cotinine antibody is linked can be effectively and safely used for the treatment of cancer.
CHIMERIC ANTIGEN RECEPTOR TO WHICH ANTI-COTININE ANTIBODY IS LINKED, AND USE THEREOF
A chimeric antibody receptors with anti-cotinine antibodies linked, and uses thereof are disclosed. A T cell presenting the chimeric antibody receptor on the surface secretes interferon gamma specifically for a target molecule of a cotinine-conjugated binding molecule that is added together therewith and induces cell death of the cell expressing the target molecule by the T cell. On the contrary, by administering a cytotoxic agent conjugated with cotinine, cell death of the chimeric antigen receptor T cell is induced. Therefore, if necessary, a cytotoxic agent conjugated with cotinine can be administered to remove the chimeric antigen receptor T cells that have been already administered, thereby suppressing immune side effects due to hyperactivity of T cells. Thus, the chimeric antigen receptor to which the anti-cotinine antibody is linked can be effectively and safely used for the treatment of cancer.
Methods and compositions for treating celiac disease
The invention features the treatment of gastrointestinal disorders associated with an innate immune response triggered by alpha amylase inhibitor CM3, alpha amylase inhibitor 0.19 (0.19), CM1, CM2, CMa, CMd, CM 16, CMb, CMX1/CMX3, CMX2, and/or alpha amylase inhibitor 0.53 (0.53). To this end, the invention features pharmaceutical compositions including neutralizing antibodies to CM3, 0.19, CM1, CM2, CMa, CMd, CM16, CMb, CMX1/CMX3, CMX2, and/or 0.53, food products containing reduced levels of CM3, 0.19, CM1, CM2, CMa, CMd, CM1 6, CMb, CMX1/CMX3, CMX2, and/or 0.53 protein, the use of oral TLR4 inhibitors to block the effect of said alpha-amylase inhibitors, assays for identifying CM3, 0.19, CM1, CM2, CMa, CMd, CM16, CMb, CMX1/CMX3, CMX2, and/or 0.53 content in food products, and assays for diagnosing subjects with a disorder related to CM3, 0.19, CM1, CM2, CMa, CMd, CM 16, CMb, CMX1/CMX3, CMX2, and/or 0.53 triggered innate immune responses.
Methods and compositions for treating celiac disease
The invention features the treatment of gastrointestinal disorders associated with an innate immune response triggered by alpha amylase inhibitor CM3, alpha amylase inhibitor 0.19 (0.19), CM1, CM2, CMa, CMd, CM 16, CMb, CMX1/CMX3, CMX2, and/or alpha amylase inhibitor 0.53 (0.53). To this end, the invention features pharmaceutical compositions including neutralizing antibodies to CM3, 0.19, CM1, CM2, CMa, CMd, CM16, CMb, CMX1/CMX3, CMX2, and/or 0.53, food products containing reduced levels of CM3, 0.19, CM1, CM2, CMa, CMd, CM1 6, CMb, CMX1/CMX3, CMX2, and/or 0.53 protein, the use of oral TLR4 inhibitors to block the effect of said alpha-amylase inhibitors, assays for identifying CM3, 0.19, CM1, CM2, CMa, CMd, CM16, CMb, CMX1/CMX3, CMX2, and/or 0.53 content in food products, and assays for diagnosing subjects with a disorder related to CM3, 0.19, CM1, CM2, CMa, CMd, CM 16, CMb, CMX1/CMX3, CMX2, and/or 0.53 triggered innate immune responses.
Enhancing activity of CAR T cells by co-introducing a bispecific antibody
The present invention provides compositions and methods for treating cancer in a human. The invention includes administering a T cell, genetically modified to express a chimeric antigen receptor (CAR), a bispecific antibody, or a combination thereof to a subject. The CAR and bispecific antibody of the invention can comprise a human antibody, a humanized antibody, or antigen-binding fragments thereof.
ANTI-HLA-DQ2.5 ANTIBODY AND ITS USE FOR THE TREATMENT OF CELIAC DISEASE
The present invention relates to anti-HLA-DQ2.5 antibodies and its use for the treatment of celiac disease.
The present invention provides anti-HLA-DQ2.5 antibodies that have been modified. The anti-HLA-DQ2.5 antibodies of the invention have binding activity to complexes formed by HLA-DQ2.5 and a gluten peptide, but have substantially no binding activity to complexes formed by HLA-DQ2.5 and an irrelevant peptide. Furthermore, the antibodies of the invention are shown to have inhibitory effects on T cell activation by gluten peptides.