PMID- 32839884
OWN - NLM
STAT- MEDLINE
DCOM- 20201102
LR  - 20240329
IS  - 1539-0829 (Electronic)
IS  - 1534-4827 (Print)
IS  - 1534-4827 (Linking)
VI  - 20
IP  - 9
DP  - 2020 Aug 25
TI  - Early Onset of Autoimmune Diabetes in Children with Down Syndrome-Two Separate 
      Aetiologies or an Immune System Pre-Programmed for Autoimmunity?
PG  - 47
LID - 10.1007/s11892-020-01318-8 [doi]
LID - 47
AB  - PURPOSE OF REVIEW: An increased frequency of autoimmunity in children with Down 
      syndrome (DS) is well described but few studies have investigated the underlying 
      mechanisms. Recent immune system investigation of individuals with DS may shed 
      light on the increased risk of autoimmune conditions including type 1 diabetes. 
      RECENT FINDINGS: Diagnosis of type 1 diabetes is accelerated in children with DS 
      with 17% diagnosed at, or under, the age of 2 years compared with only 4% in the 
      same age group in the general population. Counterintuitively, children with DS 
      and diabetes have less human leukocyte antigen (HLA)-mediated susceptibility than 
      age-matched children with autoimmune diabetes from the general population. Early 
      onset of diabetes in DS is further highlighted by the recent description of 
      neonatal cases of diabetes which is autoimmune but not HLA associated. There are 
      two potential explanations for this accelerated onset: (1) an additional 
      chromosome 21 increases the genetic and immunological risk of autoimmune diabetes 
      or (2) there are two separate aetiologies in children with DS and diabetes. 
      Autoimmunity in DS is an under-investigated area. In this review, we will draw on 
      recent mechanistic studies in individuals with DS which shed some light on the 
      increased risk of autoimmunity in children with DS and consider the current 
      support for and against two aetiologies underlying diabetes in children with DS.
FAU - Mortimer, Georgina L
AU  - Mortimer GL
AD  - Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, 
      Southmead Hospital, University of Bristol, Bristol, BS10 5NB, UK.
FAU - Gillespie, Kathleen M
AU  - Gillespie KM
AD  - Diabetes and Metabolism, Bristol Medical School, Level 2, Learning and Research, 
      Southmead Hospital, University of Bristol, Bristol, BS10 5NB, UK. 
      k.m.gillespie@bristol.ac.uk.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20200825
PL  - United States
TA  - Curr Diab Rep
JT  - Current diabetes reports
JID - 101093791
RN  - 0 (Autoantibodies)
RN  - 0 (Histocompatibility Antigens Class II)
SB  - IM
MH  - Autoantibodies
MH  - Autoimmunity
MH  - Child
MH  - *Diabetes Mellitus, Type 1/complications
MH  - *Down Syndrome/complications
MH  - Histocompatibility Antigens Class II
MH  - Humans
MH  - Immune System
MH  - *Islets of Langerhans
PMC - PMC7445156
OTO - NOTNLM
OT  - Autoimmunity
OT  - Down syndrome
OT  - HLA
OT  - Islet autoantibodies
OT  - Type 1 diabetes (T1D)
COIS- The authors declare that they have no conflict of interest.
EDAT- 2020/08/26 06:00
MHDA- 2020/11/03 06:00
PMCR- 2020/08/25
CRDT- 2020/08/26 06:00
PHST- 2020/08/26 06:00 [entrez]
PHST- 2020/08/26 06:00 [pubmed]
PHST- 2020/11/03 06:00 [medline]
PHST- 2020/08/25 00:00 [pmc-release]
AID - 10.1007/s11892-020-01318-8 [pii]
AID - 1318 [pii]
AID - 10.1007/s11892-020-01318-8 [doi]
PST - epublish
SO  - Curr Diab Rep. 2020 Aug 25;20(9):47. doi: 10.1007/s11892-020-01318-8.