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Lanreotide binds to the same receptors as somatostatin, although with higher affinity to peripheral receptors, and has similar activity. However, while somatostatin is quickly broken down in the body (within minutes), [7] lanreotide has a much longer half-life, and produces far more prolonged effects. [medical citation needed]
An autoantibody is an antibody (a type of protein) produced by the immune system that is directed against one or more of the individual's own proteins. Many autoimmune diseases (notably lupus erythematosus ) are associated with such antibodies.
As somatostatin can cause inhibition of hormone production that uses it as a mediating hormone, it has an antiproliferative effect on cell tumors, especially in neuroendocrine tumors. [2] Somatostatin analogue therapy uses longer-acting agonists than the endogenous somatostatin to extend the antiproliferative effects. [24]
It is a non-selective somatostatin receptor antagonist, [37] inhibiting the effects of somatostatin on target cells in the gastrointestinal tract, pancreas, hypothalamus, and central nervous system. [2] Cyclosomatostatin is used as a research chemical to investigate the effects of somatostatin on different cell types by antagonizing its ...
Each antibody binds to a specific antigen in a highly specific interaction analogous to a lock and key.. An antibody (Ab) or immunoglobulin (Ig) is a large, Y-shaped protein belonging to the immunoglobulin superfamily which is used by the immune system to identify and neutralize antigens such as bacteria and viruses, including those that cause disease.
Anti-topoisomerase antibodies (ATA) are autoantibodies directed against topoisomerase and found in several diseases, most importantly scleroderma. Diseases with ATA are autoimmune disease because they react with self-proteins. They are also referred to as anti-DNA topoisomerase I antibody (anti-topo I).
A new study found that in about 10% cases of multiple sclerosis, the body begins producing a distinctive set of antibodies against its own proteins years before symptoms emerge.
While the exact pathophysiology of Chagas disease is not completely understood, some models have shown that an overstimulation of the immune system causes production of adrenergic autoantibodies. Current research is trying to determine the exact role of these autoantibodies and whether they correlate with the symptomatology of Chagas disease ...