| Innate immunity and its role in type 1 diabetes. | |
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MedLine Citation:
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PMID: 18594272 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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. |
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Authors:
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Danny Zipris |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Current opinion in endocrinology, diabetes, and obesity Volume: 15 ISSN: 1752-2978 ISO Abbreviation: - Publication Date: 2008 Aug |
Date Detail:
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Created Date: 2008-07-02 Completed Date: 2008-10-31 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 101308636 Medline TA: Curr Opin Endocrinol Diabetes Obes Country: England |
Other Details:
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Languages: eng Pagination: 326-31 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, Barbara Davis Center for Childhood Diabetes, University of Colorado, Aurora, Colorado 80045-6511, USA. danny.zipris@uchsc.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Diabetes Mellitus, Type 1 / immunology*, metabolism, prevention & control Humans Immunity, Innate* Mice Models, Animal Rats Signal Transduction Toll-Like Receptors / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Toll-Like Receptors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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