PMID- 34299114
OWN - NLM
STAT- MEDLINE
DCOM- 20210730
LR  - 20210730
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 22
IP  - 14
DP  - 2021 Jul 13
TI  - The Multifactorial Progression from the Islet Autoimmunity to Type 1 Diabetes in 
      Children.
LID - 10.3390/ijms22147493 [doi]
LID - 7493
AB  - 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.
FAU - Bauer, Witold
AU  - Bauer W
AUID- ORCID: 0000-0003-0776-6714
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland.
FAU - Gyenesei, Attila
AU  - Gyenesei A
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland.
AD  - Szentagothai Research Centre, University of Pecs, Ifjusag utja 20, 7624 Pecs, 
      Hungary.
FAU - Kretowski, Adam
AU  - Kretowski A
AUID- ORCID: 0000-0002-4522-4978
AD  - Clinical Research Centre, Medical University of Bialystok, Marii 
      Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland.
AD  - Department of Endocrinology, Diabetology and Internal Medicine, Medical 
      University of Bialystok, Marii Sklodowskiej-Curie 24a, 15-276 Bialystok, Poland.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210713
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Autoantibodies)
SB  - IM
MH  - Autoantibodies/*immunology
MH  - *Autoimmunity
MH  - Child
MH  - Diabetes Mellitus, Type 1/etiology/metabolism/*pathology
MH  - *Gastrointestinal Microbiome
MH  - *Genetic Predisposition to Disease
MH  - Humans
MH  - Islets of Langerhans/immunology/metabolism/*pathology
MH  - Risk Factors
PMC - PMC8305179
OTO - NOTNLM
OT  - HLA
OT  - T1D prediction
OT  - gut microbiome
OT  - islet autoantibodies
OT  - type 1 diabetes
COIS- The authors declare no conflict of interest.
EDAT- 2021/07/25 06:00
MHDA- 2021/07/31 06:00
PMCR- 2021/07/13
CRDT- 2021/07/24 01:02
PHST- 2021/06/16 00:00 [received]
PHST- 2021/07/04 00:00 [revised]
PHST- 2021/07/09 00:00 [accepted]
PHST- 2021/07/24 01:02 [entrez]
PHST- 2021/07/25 06:00 [pubmed]
PHST- 2021/07/31 06:00 [medline]
PHST- 2021/07/13 00:00 [pmc-release]
AID - ijms22147493 [pii]
AID - ijms-22-07493 [pii]
AID - 10.3390/ijms22147493 [doi]
PST - epublish
SO  - Int J Mol Sci. 2021 Jul 13;22(14):7493. doi: 10.3390/ijms22147493.