Abstract: Certain embodiments of the disclosure relate to targeted binding agents that specifically bind to JAM-like protein and therein inhibit epithelial damage. Although it is not intended that embodiments of the disclosure be limited by any particular mechanism, it is believed that a possible mechanism by which this can be achieved may include, but are not limited to, either inhibition of binding of JAML to the CAR, inhibition of JAML induced CAR signaling, or increased clearance of JAML from the body of a subject, therein reducing the effective concentration of soluble JAML. In certain embodiment, the specific binding agent is a fully human antibody or chimera that specifically binds to human JAML, such as the JAML D1, and prevents JAML binding to CAR. Certain embodiments of the disclosure contemplate antibodies comprising human IgG type, e.g., IgG1, IgG2, IgG3, and IgG4.

Abstract: Certain embodiments of the disclosure relate to targeted binding agents that specifically bind to JAM-like protein and therein inhibit epithelial damage. Although it is not intended that embodiments of the disclosure be limited by any particular mechanism, it is believed that a possible mechanism by which this can be achieved may include, but are not limited to, either inhibition of binding of JAML to the CAR, inhibition of JAML induced CAR signaling, or increased clearance of JAML from the body of a subject, therein reducing the effective concentration of soluble JAML. In certain embodiment, the specific binding agent is a fully human antibody or chimera that specifically binds to human JAML, such as the JAML D1, and prevents JAML binding to CAR. Certain embodiments of the disclosure contemplate antibodies comprising human IgG type, e.g., IgG1, IgG2, IgG3, and IgG4.

Abstract: Certain embodiments of the disclosure relate to targeted binding agents that specifically bind to JAM-like protein and therein inhibit epithelial damage. Although it is not intended that embodiments of the disclosure be limited by any particular mechanism, it is believed that a possible mechanism by which this can be achieved may include, but are not limited to, either inhibition of binding of JAML to the CAR, inhibition of JAML induced CAR signaling, or increased clearance of JAML from the body of a subject, therein reducing the effective concentration of soluble JAML. In certain embodiment, the specific binding agent is a fully human antibody or chimera that specifically binds to human JAML, such as the JAML D1, and prevents JAML binding to CAR. Certain embodiments of the disclosure contemplate antibodies comprising human IgG type, e.g., IgG1, IgG2, IgG3, and IgG4.

Abstract: Disclosed are specific binding agents such as antibodies and chimera that bind to JAM-like protein. Also disclosed are heavy chain fragments, light chain fragments, and CDRs of the antibodies, as well as methods related thereto.

Abstract: Disclosed are specific binding agents such as antibodies and chimera that bind to JAM-like protein. Also disclosed are heavy chain fragments, light chain fragments, and CDRs of the antibodies, as well as methods related thereto.

Abstract: Polypeptides that can modulate SIRP?-CD47 functions and methods of use of the polypeptides are presented. In addition, polynucleotides that encode the polypeptides referred to above are presented. Further, pharmaceutical compositions to treat conditions are presented.

Abstract: Polypeptides that can modulate SIRP&agr;-CD47 functions and methods of use of the polypeptides are presented. In addition, polynucleotides that encode the polypeptides referred to above are presented. Further, pharmaceutical compositions to treat conditions are presented.