PMID- 28509690
OWN - NLM
STAT- MEDLINE
DCOM- 20180319
LR  - 20181202
IS  - 1752-2978 (Electronic)
IS  - 1752-296X (Print)
IS  - 1752-296X (Linking)
VI  - 24
IP  - 4
DP  - 2017 Aug
TI  - Genetics and its potential to improve type 1 diabetes care.
PG  - 279-284
LID - 10.1097/MED.0000000000000347 [doi]
AB  - PURPOSE OF REVIEW: The genetic basis of type 1 diabetes (T1D) is being 
      characterized through DNA sequence variation and cell type specificity. This 
      review discusses the current understanding of the genes and variants implicated 
      in risk of T1D and how genetic information can be used in prediction, 
      intervention and components of clinical care. RECENT FINDINGS: Fine mapping and 
      functional studies has provided resolution of the heritable basis of T1D risk, 
      incorporating novel insights on the dominant role of human leukocyte antigen 
      (HLA) genes as well as the lesser impact of non-HLA genes. Evaluation of 
      T1D-associated single nucleotide polymorphisms (SNPs), there is enrichment of 
      genetic effects restricted to specific immune cell types (CD4 and CD8 T cells, 
      CD19 B cells and CD34 stem cells), suggesting pathways to improved prediction. In 
      addition, T1D-associated SNPs have been used to generate genetic risk scores 
      (GRS) as a tool to distinguish T1D from type 2 diabetes (T2D) and to provide 
      prediagnostic data to target those for autoimmunity screening (e.g. islet 
      autoantibodies) as a prelude for continuous monitoring and entry into 
      intervention trials. SUMMARY: Genetic susceptibility accounts for nearly one-half 
      of the risk for T1D. Although the T1D-associated SNPs in white populations 
      account for nearly 90% of the genetic risk, with high sensitivity and 
      specificity, the low prevalence of T1D makes the T1D GRS of limited utility. 
      However, identifying those with highest genetic risk may permit early and 
      targeted immune monitoring to diagnose T1D months prior to clinical onset.
FAU - Rich, Stephen S
AU  - Rich SS
AD  - Center for Public Health Genomics and Department of Public Health Sciences, 
      University of Virginia, Charlottesville, Virginia, USA.
LA  - eng
GR  - Wellcome Trust/United Kingdom
GR  - U01 DK062418/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
PL  - England
TA  - Curr Opin Endocrinol Diabetes Obes
JT  - Current opinion in endocrinology, diabetes, and obesity
JID - 101308636
SB  - IM
MH  - Diabetes Mellitus, Type 1/diagnosis/*genetics/*therapy
MH  - Disease Progression
MH  - Genetic Predisposition to Disease
MH  - Genetic Testing/*methods
MH  - Humans
MH  - *Molecular Diagnostic Techniques/methods
MH  - Polymorphism, Single Nucleotide
MH  - *Precision Medicine/methods/trends
MH  - *Quality Improvement
MH  - Risk Factors
PMC - PMC6107086
MID - NIHMS941718
COIS- Conflicts of interest There are no conflicts of interest.
EDAT- 2017/05/17 06:00
MHDA- 2018/03/20 06:00
PMCR- 2018/08/23
CRDT- 2017/05/17 06:00
PHST- 2017/05/17 06:00 [pubmed]
PHST- 2018/03/20 06:00 [medline]
PHST- 2017/05/17 06:00 [entrez]
PHST- 2018/08/23 00:00 [pmc-release]
AID - 10.1097/MED.0000000000000347 [doi]
PST - ppublish
SO  - Curr Opin Endocrinol Diabetes Obes. 2017 Aug;24(4):279-284. doi: 
      10.1097/MED.0000000000000347.