Abstract: The present invention provides methods for detecting insulin autoantibody. Such methods can be used, for example, to predict susceptibility of and/or diagnose the presence of Type 1 diabetes in a subject. Some aspects of the invention also provide kits adapted for use in such methods. In particular, some aspects of the invention use proinsulin to detect the presence of insulin autoantibody.

Abstract: The present invention provides methods for detecting insulin autoantibody. Such methods can be used, for example, to predict susceptibility of and/or diagnose the presence of Type 1 diabetes in a subject. Some aspects of the invention also provide kits adapted for use in such methods. In particular, some aspects of the invention use proinsulin to detect the presence of insulin autoantibody.

Abstract: A 69 kD protein, designated PM-1, is expressed in human pancreatic islet cells and a human insulinoma. The amino acid sequence of the protein has been determined. Autoantibodies to the PM-1 protein have been found in sera of prediabetic patients. Natural, synthetic or recombinant forms of the PM-1 protein can be used in immunochemical assays to detect anti-PM-1-autoantibodies and to identify patients at risk of developing diabetes.

Abstract: A 69 kD protein, designated PM-1, is expressed in human pancreatic islet cells and a human insulinoma. The amino acid sequence of the protein has been determined. Autoantibodies to the PM-1 protein have been found in sera of prediabetic patients. Natural, synthetic or recombinant forms of the PM-1 protein can be used in immunochemical assays to detect anti-PM-1-autoantibodies and to identify patients at risk of developing diabetes.

Abstract: A 69 kD protein, designated PM-1, is expressed in human pancreatic islet cells and a human insulinoma. The amino acid sequence of the protein has been determined. Autoantibodies to the PM-1 protein have been found in sera of prediabetic patients. Natural, synthetic or recombinant forms of the PM-1 protein can be used in immunochemical assays to detect anti-PM-1-autoantibodies and to identify patients at risk of developing diabetes.

Abstract: A therapeutic agent that includes a purified peptide bound to a cytotoxic moiety, the peptide being specifically reactive with human insulin autoantibodies and non-reactive with human insulin cell surface receptor, is disclosed.

Abstract: Two subsets of Islet Cell Autoantibodies (ICA), termed restricted and non-restricted, have been identified. The expression of non-restricted ICA correlates with progression to type I diabetes, indicating that these individuals are at much greater risk than are individuals expressing restricted ICA. Differentiation between restricted or non-restricted ICA allows for more accurate prognosis of the development of type I diabetes. Restricted ICA react with beta cells of human and rat islets but not mouse, whereas non-restricted ICA react with humans rat and mouse islets. Restricted ICA can be substantially completely absorbed by incubation with glutamic acid decarboxylase (GAD), whereas non-restricted ICA are partially or not at all absorbed by GAD. Restricted ICA react in a Stiff-Man Syndrome fashion including staining GABAergic neurons in brain sections and western blots of brain extracts, whereas non-restricted ICA does not react with either brain sections nor with GAD antigen in western blots.