التفاصيل البيبلوغرافية
| العنوان: |
The role of interferon induced with helicase C domain 1 (IFIH1) in the development of type 1 diabetes mellitus |
| المؤلفون: |
Bouças,Ana Paula, Oliveira,Fernanda dos Santos de, Canani,Luis Henrique, Crispim,Daisy |
| المصدر: |
Arquivos Brasileiros de Endocrinologia & Metabologia v.57 n.9 2013 |
| بيانات النشر: |
Sociedade Brasileira de Endocrinologia e Metabologia |
| سنة النشر: |
2013 |
| المجموعة: |
SciELO Brazil (Scientific Electronic Library Online) |
| مصطلحات موضوعية: |
Autoimmunity, type 1 diabetes mellitus, viral infection, IFIH1 |
| الوصف: |
Type 1 diabetes mellitus (T1DM) is a chronic, progressive, autoimmune disease characterized by metabolic decompensation frequently leading to dehydration and ketoacidosis. Viral pathogens seem to play a major role in triggering the autoimmune destruction that leads to the development of T1DM. Among several viral strains investigated so far, enteroviruses have been consistently associated with 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 IFIH1 gene encodes a cytoplasmic receptor of the pattern-recognition receptors (PRRs) family that recognizes dsRNA, playing a role in the innate immune response triggered by viral infection. Binding of dsRNA to this PRR triggers the release of proinflammatory cytokines, such as interferons (IFNs), which exhibit potent antiviral activity, protecting uninfected cells and inducing apoptosis of infected cells. The IFIH1 gene appears to play a major role in the development of some autoimmune diseases, and it is, therefore, a candidate gene for T1DM. Within this context, the objective of the present review was to address the role of IFIH1 in the development of T1DM. |
| نوع الوثيقة: |
article in journal/newspaper |
| وصف الملف: |
text/html |
| اللغة: |
English |
| الإتاحة: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302013000900001Test |
| رقم الانضمام: |
edsbas.F543AF10 |
| قاعدة البيانات: |
BASE |
