Diabetes associated with autoimmune pancreatitis: new insights into the mechanism of β-cell dysfunction

Abstract

A high proportion of patients with autoimmune pancreatitis (AIP) have diabetes. The decreased β-cell function in active AIP, which leads to diabetes, can sometimes be reversed by corticosteroid treatment. However, the immunological mechanisms causing this β-cell dysfunction are largely unclear. Our recent studies on AIP complicated with diabetes, and data from other animal models of AIP, suggest the presence of distinct mechanisms responsible for β-cell damage in AIP. The presence of immunological cross-reactivity against antigens that are localized both in exocrine pancreatic tissue and β-cells may explain the concomitant occurrence of pancreatitis and β-cell damage in AIP.

Keywords::

• amylase
• autoantibodies
• autoimmune pancreatitis
• β-cells
• diabetes
• fulminant Type 1 diabetes
• HLA
• IgG4
• insulitis
• peri-insulitis
• Treg

Acknowledgements

We wish to thank Kaori Hosaka, Chihiro Imai and Sachiko Takei for excellent secretarial work, and Kazuo Takeuchi of the Department of Gastroenterology, Toranomon Hospital and Hideki Fujii of the First Department of Surgery at the University of Yamanashi for their generous help with this work.

Financial & competing interests disclosure

This study was partly supported by grants from the Ministry of Education, Science, Sports and Culture, Japan. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Notes

PSC: Primary sclerosing cholangitis.

Reproduced with permission from [5].