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

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 increa...

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Main Authors: James A. Pearson, Andrew Agriantonis, F. Susan Wong, Li Wen
Format: Article
Language:English
Published: Taylor & Francis Group 2018-11-01
Series:Human Vaccines & Immunotherapeutics
Subjects:
Online Access:http://dx.doi.org/10.1080/21645515.2018.1514354
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author James A. Pearson
Andrew Agriantonis
F. Susan Wong
Li Wen
author_facet James A. Pearson
Andrew Agriantonis
F. Susan Wong
Li Wen
author_sort James A. Pearson
collection DOAJ
description 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.
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spelling doaj.art-44117b47428741f190cdf93b2ef882c02023-09-22T08:38:23ZengTaylor & Francis GroupHuman Vaccines & Immunotherapeutics2164-55152164-554X2018-11-0114112580259610.1080/21645515.2018.15143541514354Modulation of the immune system by the gut microbiota in the development of type 1 diabetesJames A. Pearson0Andrew Agriantonis1F. Susan Wong2Li Wen3Yale UniversityYale UniversityCardiff UniversityYale UniversityT1D 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.http://dx.doi.org/10.1080/21645515.2018.1514354gut microbiotatype 1 diabetesnod micetherapy
spellingShingle James A. Pearson
Andrew Agriantonis
F. Susan Wong
Li Wen
Modulation of the immune system by the gut microbiota in the development of type 1 diabetes
Human Vaccines & Immunotherapeutics
gut microbiota
type 1 diabetes
nod mice
therapy
title Modulation of the immune system by the gut microbiota in the development of type 1 diabetes
title_full Modulation of the immune system by the gut microbiota in the development of type 1 diabetes
title_fullStr Modulation of the immune system by the gut microbiota in the development of type 1 diabetes
title_full_unstemmed Modulation of the immune system by the gut microbiota in the development of type 1 diabetes
title_short Modulation of the immune system by the gut microbiota in the development of type 1 diabetes
title_sort modulation of the immune system by the gut microbiota in the development of type 1 diabetes
topic gut microbiota
type 1 diabetes
nod mice
therapy
url http://dx.doi.org/10.1080/21645515.2018.1514354
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