Background: Autoimmune diseases are characterized by a breakdown of immunologic tolerance, and this breakdown can lead to life-threatening or lifelong disorders. Moreover; drugs that are used to treat these diseases are few in number and are associated with many serious adverse effects. Methods: We used the rat insulin promoter-glycoprotein mouse model to analyze the role of tunicamycin in the process of autoimmune diabetes; the P14 mouse model to analyze the effect of tunicamycin on CD8+ T cells; chop knockout mice to analyze the role of tunicamycin on an endoplasmic reticulum stress model; and fluorescence-activated cell sorting, quantitative real-time polymerase chain reaction, and histologic methods. Results: We found that a single dose of tunicamycin reduced the activation and pancreatic infiltration of CD8+ T cells. This activity delayed the incidence of virus-induced diabetes and improved survival rates. Conclusion: Tunicamycin may offer therapeutic opportunities for T cell-mediated autoimmune diseases such as diabetes.

Keywords:
Tunicamycin, Endoplasmic reticulum stress, Oxidative stress, Lymphocytic choriomeningitis virus, Diabetes
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© 2012 S. Karger AG, Basel
2012
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