The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children

Type 1 Diabetes (T1D) results from autoimmune destruction of insulin producing pancreatic ß-cells. This disease, with a peak incidence in childhood, causes the lifelong need for insulin injections and necessitates careful monitoring of blood glucose levels. However, despite the current insulin thera...

Full description

Bibliographic Details
Main Authors: Witold Bauer, Attila Gyenesei, Adam Krętowski
Format: Article
Language:English
Published: MDPI AG 2021-07-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/22/14/7493
_version_ 1797526946515517440
author Witold Bauer
Attila Gyenesei
Adam Krętowski
author_facet Witold Bauer
Attila Gyenesei
Adam Krętowski
author_sort Witold Bauer
collection DOAJ
description Type 1 Diabetes (T1D) results from autoimmune destruction of insulin producing pancreatic ß-cells. This disease, with a peak incidence in childhood, causes the lifelong need for insulin injections and necessitates careful monitoring of blood glucose levels. However, despite the current insulin therapies, it still shortens life expectancy due to complications affecting multiple organs. Recently, the incidence of T1D in childhood has increased by 3–5% per year in most developed Western countries. The heterogeneity of the disease process is supported by the findings of follow-up studies started early in infancy. The development of T1D is usually preceded by the appearance of autoantibodies targeted against antigens expressed in the pancreatic islets. The risk of T1D increases significantly with an increasing number of positive autoantibodies. The order of autoantibody appearance affects the disease risk. Genetic susceptibility, mainly defined by the human leukocyte antigen (HLA) class II gene region and environmental factors, is important in the development of islet autoimmunity and T1D. Environmental factors, mainly those linked to the changes in the gut microbiome as well as several pathogens, especially viruses, and diet are key modulators of T1D. The aim of this paper is to expand the understanding of the aetiology and pathogenesis of T1D in childhood by detailed description and comparison of factors affecting the progression from the islet autoimmunity to T1D in children.
first_indexed 2024-03-10T09:37:31Z
format Article
id doaj.art-acf920bc20964ed794c0e0ec5bf21010
institution Directory Open Access Journal
issn 1661-6596
1422-0067
language English
last_indexed 2024-03-10T09:37:31Z
publishDate 2021-07-01
publisher MDPI AG
record_format Article
series International Journal of Molecular Sciences
spelling doaj.art-acf920bc20964ed794c0e0ec5bf210102023-11-22T03:59:29ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-07-012214749310.3390/ijms22147493The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in ChildrenWitold Bauer0Attila Gyenesei1Adam Krętowski2Clinical Research Centre, Medical University of Białystok, Marii Skłodowskiej-Curie 24a, 15-276 Białystok, PolandClinical Research Centre, Medical University of Białystok, Marii Skłodowskiej-Curie 24a, 15-276 Białystok, PolandClinical Research Centre, Medical University of Białystok, Marii Skłodowskiej-Curie 24a, 15-276 Białystok, PolandType 1 Diabetes (T1D) results from autoimmune destruction of insulin producing pancreatic ß-cells. This disease, with a peak incidence in childhood, causes the lifelong need for insulin injections and necessitates careful monitoring of blood glucose levels. However, despite the current insulin therapies, it still shortens life expectancy due to complications affecting multiple organs. Recently, the incidence of T1D in childhood has increased by 3–5% per year in most developed Western countries. The heterogeneity of the disease process is supported by the findings of follow-up studies started early in infancy. The development of T1D is usually preceded by the appearance of autoantibodies targeted against antigens expressed in the pancreatic islets. The risk of T1D increases significantly with an increasing number of positive autoantibodies. The order of autoantibody appearance affects the disease risk. Genetic susceptibility, mainly defined by the human leukocyte antigen (HLA) class II gene region and environmental factors, is important in the development of islet autoimmunity and T1D. Environmental factors, mainly those linked to the changes in the gut microbiome as well as several pathogens, especially viruses, and diet are key modulators of T1D. The aim of this paper is to expand the understanding of the aetiology and pathogenesis of T1D in childhood by detailed description and comparison of factors affecting the progression from the islet autoimmunity to T1D in children.https://www.mdpi.com/1422-0067/22/14/7493type 1 diabetesT1D predictionislet autoantibodiesHLAgut microbiome
spellingShingle Witold Bauer
Attila Gyenesei
Adam Krętowski
The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
International Journal of Molecular Sciences
type 1 diabetes
T1D prediction
islet autoantibodies
HLA
gut microbiome
title The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
title_full The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
title_fullStr The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
title_full_unstemmed The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
title_short The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in Children
title_sort multifactorial progression from the islet autoimmunity to type 1 diabetes in children
topic type 1 diabetes
T1D prediction
islet autoantibodies
HLA
gut microbiome
url https://www.mdpi.com/1422-0067/22/14/7493
work_keys_str_mv AT witoldbauer themultifactorialprogressionfromtheisletautoimmunitytotype1diabetesinchildren
AT attilagyenesei themultifactorialprogressionfromtheisletautoimmunitytotype1diabetesinchildren
AT adamkretowski themultifactorialprogressionfromtheisletautoimmunitytotype1diabetesinchildren
AT witoldbauer multifactorialprogressionfromtheisletautoimmunitytotype1diabetesinchildren
AT attilagyenesei multifactorialprogressionfromtheisletautoimmunitytotype1diabetesinchildren
AT adamkretowski multifactorialprogressionfromtheisletautoimmunitytotype1diabetesinchildren