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The Role of Toll-Like Receptors 3 and 9 in the Development of Autoimmune Diabetes in NOD Mice

Authors


Address for correspondence: Li Wen, TAC-S141, Mail Box 208020, Yale University School of Medicine, 330 Cedar Street, New Haven, CT 06520. li.wen@yale.edu

Abstract

Innate immunity is mediated, at least in part, through a number of receptors known as Toll-like receptors (TLRs), which are activated by different microbial stimuli. Adaptive immunity, including autoimmunity, follows the innate response in a more specific manner. To investigate the roles of TLR3 and TLR9 in the development of type 1 diabetes, we generated NOD mice that are deficient in TLR3 and 9, respectively. There was no obvious difference in the incidence of spontaneous diabetes between TLR3-deficient mice and TLR3 heterozygous mice. However, TLR9-deficient mice were markedly protected from the disease compared to TLR9 heterozygous mice. Our results suggest that different TLRs play a varying role in autoimmune diseases.

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