Abstract:
Gliadin is identified as a physiological receptor for CXCR3. Assays for determining modulators of CXCR3 signaling are provided. Fragments of gliadin which function as inhibitors of CXCR3 signaling can be determined. Methods for treating diseases relating to gluten and/or autoimmunity by targeting CXCR3 are provided. Such diseases include celiac disease, gluten sensitivity, gluten allergy, rheumatoid arthritis, multiple sclerosis, immune-mediated or type 1 diabetes mellitus, inflammatory bowel diseases, systemic lupus erythematosus, psoriasis, scleroderma, and autoimmune thyroid diseases.
Abstract:
Gliadin is identified as a physiological receptor for CXCR3. Assays for determining modulators of CXCR3 signaling are provided. Fragments of gliadin which function as inhibitors of CXCR3 signaling can be determined. Methods for treating diseases relating to gluten and/or autoimmunity by targeting CXCR3 are provided. Such diseases include celiac disease, gluten sensitivity, gluten allergy, rheumatoid arthritis, multiple sclerosis, immune-mediated or type 1 diabetes mellitus, inflammatory bowel diseases, systemic lupus erythematosus, psoriasis, scleroderma, and autoimmune thyroid diseases.
Abstract:
The present invention is directed to a adjuvant peptide and uses to facilitate antigen absorption in the mucosa, particularly nasal tissue. Vaccine compositions for mucosal delivery include the adjuvant peptide and an antigen for inducing an immune response.
Abstract:
Agonist polypeptide of a receptor protein has been identified. The agonist can be used to facilitate drug and antigen absorption. Suitable routes of administration include oral, nasal, transdermal, and intravenous. Pharmaceutical formulations may comprise a therapeutic agent or an immunogenic agent in combination with the agonist polypeptide.
Abstract:
The present invention provides a method of treating an autoimmune disease, comprising the steps of increasing transepithelial electrical resistance leading to decreased cell permeability. Further provided is ajnethod of treating celiac disease in an individual in need of such treatment, comprising the steps of: administering an antibody directed against single chain zonulin thereby inhibiting epidermal growth factor receptor and inhibiting PAR2.
Abstract:
The present application provides compositions and methods for treating acute lung injury and acute respiratory distress syndrome. The methods include administering one or more tight junction antagonists to the lung of a subject in need thereof.
Abstract:
The present invention provides compositions and methods for the administration of the compositions to mammals. The compositions comprise therapeutic agents and an intestinal absorption enhancing amount of one or more tight junction agonists. Tight junction agonists include zonulin and/or ZOT receptor agonists. Methods of the invention include orally administering compositions of the invention.
Abstract:
The present invention provides materials and methods to facilitate the pulmonary delivery of therapeutic agents. In some embodiments, agonists of tight junctions (e.g., zonulin agonists) are used in compositions to facilitate the uptake of therapeutic agents from the pulmonary mucosa.
Abstract:
The present invention provides materials and methods for the treatment of diabetes. Using the materials and methods of the invention, the loss of pancreatic ß-cells can be slowed and/or prevented. In addition!, the materials and methods of the invention can be used to regenerate pancreatic ß-cells.
Abstract:
The present invention provides materials and methods to assess the efficacy of a treatment. In some embodiments, the present invention provides a method of assessing the efficacy of a treatment for celiac disease by measuring the serum zonulin level of a subject having received the treatment.