Nitric Oxide in the Immunopathogenesis of Type 1 Diabetes

* Final gross prices may vary according to local VAT.

Get Access

Abstract

During the past decade, research on the pathogenesis of human type 1 diabetes considerably increased our insight into the mechanisms involved in the destruction of insulin-producing β cells of pancreatic islets of Langerhans. Cell-mediated immune reactivity against islet constituents is assumed to play a major role in the development of this disease (EISENBARTH 1986). In an attempt to identify cellular effector mechanisms involved in β-cell destruction, (1991) demonstrated that nitric oxide (NO) released from activated macrophages is able to exert cytotoxic activity against islet cells. Since then, increasing research activities focused on the source, the target structures and the metabolic or cytotoxic effects of NO in the process of β-cell destruction. From the growing number of observations, a picture emerges which identifies NO as a major regulatory and cytotoxic mediator during islet inflammation. This qualifies the mechanisms involved in NO-induced β-cell death as important targets for intervention strategies aiming at the prevention of type 1 diabetes (CORBETT and MCDANIEL 1992; KOLB and KOLB-BACHOFEN 1992; BURKART et al. 1994).