Skip to main navigation Skip to search Skip to main content

Modulation of the immune system by the gut microbiota in the development of type 1 diabetes

  • James A. Pearson
  • , Andrew Agriantonis
  • , F. Susan Wong
  • , Li Wen*
  • *Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

Abstract

T1D is an autoimmune disease characterized by T cell-mediated destruction of insulin-producing β-cells in the pancreatic islets of Langerhans, resulting in hyperglycemia, with patients requiring lifelong insulin treatment. Many studies have shown that genetics alone are not sufficient for the increase in T1D incidence and thus other factors have been suggested to modify the disease risk. T1D incidence has sharply increased in the developed world, especially amongst youth. In Europe, T1D incidence is increasing at an annual rate of 3–4%. Increasing evidence shows that gut microbiota, as one of the environmental factors influencing diabetes development, play an important role in development of T1D. Here, we summarize the current knowledge about the relationship between the microbiota and T1D. We also discuss the possibility of T1D prevention by changing the composition of gut microbiota.

Original languageEnglish
Pages (from-to)2580-2596
Number of pages17
JournalHuman Vaccines and Immunotherapeutics
Volume14
Issue number11
DOIs
Publication statusPublished - 2 Nov 2018

Bibliographical note

Publisher Copyright:
© 2018, © 2018 Taylor & Francis Group, LLC.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Gut microbiota
  • NOD mice
  • therapy
  • type 1 diabetes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology

Fingerprint

Dive into the research topics of 'Modulation of the immune system by the gut microbiota in the development of type 1 diabetes'. Together they form a unique fingerprint.

Cite this