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Published VersionCC BY V4.0, Open Access
Journal article
Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus
Archives of Endocrinology and Metabolism, Vol.59(1), pp.4-12
2015
Abstract
Type 1 diabetes mellitus (T1DM) is a chronic, progressive autoimmune disease characterized by metabolic decompensation often leading to dehydration and ketoacidosis. Viral agents seem to play an important role in triggering the autoimmune destruction that leads to the development of T1DM. Among several viral strains investigated so far, the enterovirus family has been consistently associated with the onset of T1DM in humans. One of the mediators of viral damage is the double-stranded RNA (dsRNA) generated during replication and transcription of viral RNA and DNA. The Toll-like receptor 3 (TLR3) gene codes for an endoplasmic receptor of the pattern-recognition receptors (PRRs) family that recognizes dsRNA, plays an important role in the innate immune response triggered by viral infection. Binding of dsRNA to the TLR3 triggers the release of proinflammatory cytokines, such as interferons, which exhibit potent antiviral action; thus, protecting uninfected cells and inducing apoptosis of infected ones. Therefore, the TLR3 gene is a good candidate for the development of T1DM. Within this context, the objective of the present review was to address the role of the TLR3 gene in the development of T1DM.
Details
- Title
- Toll-like receptor 3 (TLR3) and the development of type 1 diabetes mellitus
- Authors
- T S Assmann (Author) - Universidade Federal do Rio Grande do SulL A Brondani (Author) - Universidade Federal do Rio Grande do SulA P Bouças (Author) - Universidade Federal do Rio Grande do SulL H Canani (Author) - Universidade Federal do Rio Grande do SulD Crispim (Author) - Universidade Federal do Rio Grande do Sul
- Publication details
- Archives of Endocrinology and Metabolism, Vol.59(1), pp.4-12
- Publisher
- Sociedade Brasileira de Endocrinologia e Metabologia
- Date published
- 2015
- DOI
- 10.1590/2359-3997000000003
- ISSN
- 2359-3997; 2359-3997
- Copyright note
- Copyright © 2015 The Authors. This article is licenced under Creative Commons: https://creativecommons.org/licenses/by/4.0/deed.en
- Organisation Unit
- Thompson Institute
- Language
- English
- Record Identifier
- 99451247002621
- Output Type
- Journal article
- Research Statement
- false
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- Domestic collaboration
- Web Of Science research areas
- Endocrinology & Metabolism
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