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.

[1][8][9] It is known that genetic and environmental factors contribute to insulitis initiation, however, the exact process that causes it is unknown.

The chemokine family of proteins may play a key role in promoting leukocytic infiltration into the pancreas prior to pancreatic beta-cell destruction.

[11] 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.

[4] 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.

[1] The exact reason for this disparity between age groups is unknown, however it is theorised that adults may have a different or less severe form of type 1 diabetes that progresses slower.

If insulitis and type 1 diabetes development was successfully detected in a non-invasive method prior to the extensive loss of insulin secreting beta cells, the administration of immunosuppressant therapy would prevent the immune cell infiltration into the islets of langerhans.

First, the pancreatectomy is performed, with the full pancreas only being removed in more extreme cases such as from debilitating pain from chronic pancreatitis, then viable islet cells are isolated and implanted into a patient's liver via the portal vein with an image-guided catheter.

[3][15] Because the implanted islet cells come from the patient's body, there is no immune rejection and no need for immunosuppressant therapy.

[2][17] Young patients were the primary focus of their research due to children having the “best examples of pure, uncomplicated diabetes mellitus,” (In't Veld, 2011) and having fewer complications that arise with age.

[2][16] In 1958, Philip LeCompte reexamined acute onset disease and short duration by studying 4 related insulitis cases.

[2][16] Further study in 1978 led Gepts to the conclusion that “insulitis represents an immune reaction of the delayed type, specifically directed against beta-cells,”(In’t Veld, 2011).