Background. The reasons for the long-term complete or partial loss of islet graft function are unknown, but there are obviously other reasons than just pure allogeneic graft rejection. Earlier studies have shown that deposition of islet amyloid polypeptide amyloid in transplanted islets may indicate a mechanism for loss of β cells.
Materials and Methods. Sections from liver material from four deceased islet-bearing recipients have been scrutinized for the presence of amyloid. Clinical data and certain aspects of the islet graft pathology of these patients have been published previously.
Result. With this extended histological analysis, we demonstrate the occurrence of amyloid deposits in islets transplanted into the liver in three of four patients with type 1 diabetes.
Conclusion. The finding adds evidence to the assumption that aggregation of islet amyloid polypeptide might be an important cause of progressing β-cell dysfunction in clinically transplanted islets.
1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden.
2Department of Medicine and Metabolic Disease, Ospedale San Raffaele, Milan, Italy.
3Diabetes Division, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX.
4Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada.
5Department of Surgery, University of Geneva Hospitals, Geneva, Switzerland.
6Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.
7Department of Surgical Sciences, Uppsala University, Uppsala, Sweden.
The work was supported by the Swedish Research Council grant 5343 (G.T.W.), 5941 (P.W.), and 12219 (O.K.), the Swedish Diabetes Association (G.T.W.), Novo Nordisk (G.T.W.), the Family Ernfors Fund (G.T.W.), NIH grant RO1 DK080148 (F.F.), Swiss National Science Foundation (SCORE) grant 3232230-126233 (C.T.), NIH-NIAID grant for the CIT network (A.M.J.S.), and through Alberta Innovates Healthcare solutions (A.M.J.S.), NIH-NIAID grant 2U01AI065192-06 for the CIT network (O.K.), and the Juvenile Diabetes Foundation International (O.K.).
The authors declare no conflicts of interest.
Address correspondence to: Gunilla T. Westermark, Ph.D., Department of Medical Cell Biology, Uppsala University, SE-75123, Uppsala, Sweden. E-mail: email@example.com
The material and clinical data were collected at three different transplant units. Because of the differences in published histopathology, we have jointly decided to perform the described work. All authors participated in the planning, implementation, and compilation of the manuscript.
Received 7 July 2011. Revision requested 6 August 2011.
Accepted 20 October 2011.