UMMS Affiliation

Department of Medicine, Division of Endocrinology and Diabetes

Publication Date


Document Type



Animals; Cyclophosphamide; Diabetes Mellitus, Type 1; Female; Immunohistochemistry; Islets of Langerhans; Mice; Mice, Inbred NOD; Receptors, Tumor Necrosis Factor, Member 10c; Streptozocin; TNF-Related Apoptosis-Inducing Ligand


Endocrine System Diseases | Immunology and Infectious Disease


TNF-related apoptosis-inducing ligand (TRAIL) is an important component of the immune system. Although it is well acknowledged that it also has an important role in Type 1 Diabetes (T1D) development, this presumed role has not yet been clearly revealed. Streptozotocin (STZ) and Cyclophosphamide (CY) are frequently used agents for establishment or acceleration of T1D disease in experimental models, including the non-obese diabetic (NOD) mice. Although such disease models are very suitable for diabetes research, different expression patterns for various T1D-related molecules may be expected, depending on the action mechanism of the applied agent. We accelerated diabetes in female NOD mice using STZ or CY and analyzed the expression profiles of TRAIL ligand and receptors throughout disease development. TRAIL ligand expression followed a completely different pattern in STZ- versus CY-accelerated disease, displaying a prominent increase in the former, while appearing at reduced levels in the latter. Decoy receptor 1 (DcR1) expression also increased significantly in the pancreatic islets in STZ-induced disease. Specific increases observed in TRAIL ligand and DcR1 expressions may be part of a defensive strategy of the beta islets against the infiltrating leukocytes, while the immune-suppressive agent CY may partly hold down this defense, contributing further to diabetes development.

Rights and Permissions

Copyright © 2011 Ercument Dirice et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

DOI of Published Version



Exp Diabetes Res. 2011;2011:625813. doi: 10.1155/2011/625813. Epub 2011 Nov 28. Link to article on publisher's site

Journal/Book/Conference Title

Experimental diabetes research

Related Resources

Link to Article in PubMed

PubMed ID