Send to:

Choose Destination
See comment in PubMed Commons below
Curr Opin Endocrinol Diabetes Obes. 2008 Aug;15(4):326-31. doi: 10.1097/MED.0b013e3283073a46.

Innate immunity and its role in type 1 diabetes.

Author information

  • 1Department of Pediatrics, Barbara Davis Center for Childhood Diabetes, University of Colorado, Aurora, Colorado 80045-6511, USA.



Over the last 2 decades, studies addressing mechanisms of type 1 diabetes have focused primarily on the role of T lymphocytes in disease mechanisms. Recent investigations, however, suggest that the innate immune system plays a key role in promoting the response of autoreactive T cells triggering type 1 diabetes. The discovery of toll-like receptors in the 1990s has led to a better understanding of signaling pathways involved in initiating innate immune pathways and how these pathways may be associated with mechanisms leading to autoimmune disease. This review focuses on recent studies on the role of Toll-like receptors and innate pathways in triggering type 1 diabetes.


Data from animal models of type 1 diabetes provide strong support to the hypothesis that Toll-like receptor-induced innate signaling pathways are involved in the proinflammatory process leading to autoimmune diabetes. Studies performed in peripheral blood cells and sera from patients with type 1 diabetes indicate that aberrant innate functions might exist in such patients, but the relevance of these alterations to the mechanism leading to type 1 diabetes is currently unclear.


The discovery that innate signaling pathways are involved in the mechanism that may trigger islet inflammation and destruction holds great promise for the identification of new innate signaling molecules that could be targeted to specifically inhibit the autoimmune process to prevent autoimmune diabetes.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Write to the Help Desk