Abstract: Anti-Kv1.3 antibodies (mAbs), particularly mAbs that specifically bind to Kv1.3 with high affinity and/or inhibit Kv1.3 function, are disclosed. The amino acid sequences of the CDRs of the light chains and the heavy chains, as well as consensus sequences for these CDRs, of these anti-Kv1.3 mAbs are provided. Additionally, canonical structures for CDRs in the VH and VL regions of anti-Kv1.3 antibodies are provided. The disclosure also provides nucleic acid molecules encoding the anti-Kv1.3 mAbs, expression vectors, host cells, methods for making the anti-Kv1.3 mAbs, and methods for expressing the anti-Kv1.3 mAbs. Finally, methods of using the anti-Kv1.3 mAbs as therapeutics, such as for preventing or treating an autoimmune disorder, are disclosed.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.

Abstract: Anti-Kv1.3 antibodies (mAbs), particularly mAbs that specifically bind to Kv1.3 with high affinity and/or inhibit Kv1.3 function, are disclosed. The amino acid sequences of the CDRs of the light chains and the heavy chains, as well as consensus sequences for these CDRs, of these anti-Kv1.3 mAbs are provided. Additionally, canonical structures for CDRs in the VH and VL regions of anti-Kv1.3 antibodies are provided. The disclosure also provides nucleic acid molecules encoding the anti-Kv1.3 mAbs, expression vectors, host cells, methods for making the anti-Kv1.3 mAbs, and methods for expressing the anti-Kv1.3 mAbs. Finally, methods of using the anti-Kv1.3 mAbs as therapeutics, such as for preventing or treating an autoimmune disorder, are disclosed.

Abstract: The present invention relates to antibodies and antigen binding fragments thereof, which bind to a complex of GARP and TGF-?1, particularly a complex of human GARP and human TGF-?1. These antibodies and antigen binding fragments exhibit a combination of advantageous properties including high affinity antigen binding and the ability to inhibit the release of active TGF-? from regulatory T cells. The antibodies and antigen binding fragments of the present invention are relatively resistant to deamidation, isomerization and oxidation, such that they display improved stability.