Type I Diabetes is mainly characterised by limited or fully missing secretion of the hormone insulin. Morphological studies demonstrated a destruction of the beta cells of the so-called Langerhans cells (islet cells) in type I diabetics. Numerous researchers described the appearance of antibodies directed against the islet cells and insulin as the causal reason for the onset of the disease.
Anti-Insulin antibodies are found in 37 percent of patients with newly detected Type I Diabetes, in 4 percent of their relatives of the first degree and in up to 1.5 percent of healthy controls. A positive correlation between the appearance of anti-Insulin and anti-islet cell antibodies has been reported. Anti-Insulin autoantibodies may be detected several months and in some cases years before the onset of the fully clinical manifestation of the diseases. Occasionally also autoantibodies to Pro-Insulin may appear.
These ''true'' anti-Insulin autoantibodies directed against endogenous insulin have to be distinguished from those autoantibodies which are developed in insulin dependent diabetics undergoing therapy with insulin preparations of animal origin. In fact the latter have to be referred to side effects. These side effects may occur as local reactions of the skin by development of insulin-specific autoantibodies. These autoantibodies are causing the formation of an insulin depot and they may simulate a resistance against the hormonal treatment with animal insulin. Additionally other immunological phenomenon have been reported for Type I diabetics. A lot of other autoantibody specificities have been detected in those patients, too, but these antibodies must not cause additional autoimmune phenomenon.
INHBB; inhibin, beta B; inhibin, beta B (activin AB beta polypeptide); inhibin beta B chain; Inhibin, beta-2; activin beta-B chain; activin AB beta polypeptide; MGC157939; activin beta B; actbb; actbetaB