Altered immune regulation in type 1 diabetes

András Zóka, Györgyi Muzes, Anikó Somogyi, Tímea Varga, Barbara Szémán, Zahra Al-Aissa, Orsolya Hadarits, Gábor Firneisz

Research output: Contribution to journalReview article

12 Citations (Scopus)

Abstract

Research in genetics and immunology was going on separate strands for a long time. Type 1 diabetes mellitus might not be characterized with a single pathogenetic factor. It develops when a susceptible individual is exposed to potential triggers in a given sequence and timeframe that eventually disarranges the fine-tuned immune mechanisms that keep autoimmunity under control in health. Genomewide association studies have helped to understand the congenital susceptibility, and hand-in-hand with the immunological research novel paths of immune dysregulation were described in central tolerance, apoptotic pathways, or peripheral tolerance mediated by regulatory T-cells. Epigenetic factors are contributing to the immune dysregulation. The interplay between genetic susceptibility and potential triggers is likely to play a role at a very early age and gradually results in the loss of balanced autotolerance and subsequently in the development of the clinical disease. Genetic susceptibility, the impaired elimination of apoptotic β-cell remnants, altered immune regulatory functions, and environmental factors such as viral infections determine the outcome. Autoreactivity might exist under physiologic conditions and when the integrity of the complex regulatory process is damaged the disease might develop. We summarized the immune regulatory mechanisms that might have a crucial role in disease pathology and development.

Original languageEnglish
Article number254874
JournalClinical and Developmental Immunology
Volume2013
DOIs
Publication statusPublished - Sep 23 2013

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Altered immune regulation in type 1 diabetes'. Together they form a unique fingerprint.

  • Cite this