insulitis

Insulitis is an inflammation of the islets of Langerhans, a collection of endocrine tissue located in the pancreas that helps regulate glucose levels, and is classified by specific targeting of immune cell (T and B lymphocytes, macrophages and dendritic cells) infiltration in the islets of Langerhans. This immune cell infiltration can result in the destruction of insulin-producing beta cells of the islets, which plays a major role in the pathogenesis, the disease development, of type 1 and type 2 diabetes. Insulitis is present in 19% of individuals with type 1 diabetes and 28% of individuals with type 2 diabetes. It is known that genetic and environmental factors contribute to insulitis initiation, however, the exact process that causes it is unknown. Insulitis is often studied using the non-obese diabetic (NOD) mouse model of type 1 diabetes. The chemokine family of proteins may play a key role in promoting leukocytic infiltration into the pancreas prior to pancreatic beta-cell destruction.

== Pathophysiology == The pathogenesis of insulitis can be assessed based on the threshold of CD3+ or CD45+ cells surrounding or infiltrating the islets of Langerhans, however, this can only be studied with a pancreatic tissue sample. CD3+ and CD45+ (cluster of differentiation 3 & 45 positive cells) are lymphocytes. Studying non-obese diabetic mice has revealed a correlation between insulitis progression and quantity of insulin autoantibodies production in the blood circulation, as well as a link between certain combinations of present autoantibodies and risk for developing type 1 diabetes and insulitis.