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Epigenetics in autoimmune diseases with focus on type 1 diabetes

Authors

  • Mary Ngoc Dang,

    1. Centre for Diabetes and Metabolic Medicine, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, UK
    2. Department of Endocrinology and Diabetes, University Campus Bio-Medico of Rome, Italy
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  • Raffaella Buzzetti,

    1. Department of Experimental Medicine, Sapienza University, Rome, Italy
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  • Paolo Pozzilli

    Corresponding author
    1. Centre for Diabetes and Metabolic Medicine, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary, University of London, UK
    • Department of Endocrinology and Diabetes, University Campus Bio-Medico of Rome, Italy
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Paolo Pozzilli, University Campus Bio-Medico, Via Alvaro del Portillo, 21 00128 Rome, Italy.

E-mail: p.pozzilli@unicampus.it

Summary

Autoimmune diseases arise when the body mounts an immune response against ‘self’ cells and tissues causing inflammation and damage. It is commonly accepted that these diseases develop because of the interplay of genetic and environmental factors. Evidence for genetic factors includes the higher concordance of disease in monozygotic twins than in dizygotic twins. However, monozygotic twins may remain discordant for disease indicating a role for environmental factors. Environmental factors may alter gene expression via epigenetic mechanisms. This is particularly pertinent in type 1 diabetes in which DNA methylation and histone modifications have been associated with altered gene expression. The low disease concordance rate in adult-onset type 1 diabetes (<20%) suggests that environmental and epigenetic changes may play a predominant role. Defining the role of epigenetic changes could identify specific gene pathways and dysregulated expression of gene products that contribute to the pathogenesis of type 1 diabetes. This article reviews how epigenetic mechanisms may contribute to the development of autoimmune diseases with a focus on type 1 diabetes. Copyright © 2012 John Wiley & Sons, Ltd.

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