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The most successful window of opportunity for diabetes prevention in NOD mice is between points A and C.

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Legend:

Ag: antigen
APC: antigen-presenting cell
CTLA4: cytotoxic T lymphocyte antigen-4
GAD85: glutamic acid decarboxylase 85
HLA: human leukocyte antigen
IA2: islet antigen-2
IAPP: islet amyloid polypeptide
IFIH: interferon induced helicase
IFNa: interferon alpha
IFNg: interferon gamma
IGRP: islet-specific glucose-6-phosphatase catalytic subunit-related protein
IL2Ra: interleukin 2 receptor subunit alpha
LN: lymph node
MHC I: major histocompatibility complex
Preproinsulin SP: preproinsulin signal peptide
PTPN22: protein tyrosine phosphatase, non-receptor type 22
TNFa: Tumor necrosis factor-alpha
Treg: regulatory T cell
ZnT8: zinc transporter 8

When we go to humans, most of the time we do our interventions very late, when autoantibodies are already present and where the immune system is already activated and is already destroying the beta cells. And so, an important lesson that we can learn from human interventions, but also the NOD interventions is that perhaps, yes, there are some criticisms of the NOD mouse model but also, perhaps, that our timing of intervention is not appropriate.
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van Belle TL, Coppieters KT, von Herrath MG. Type 1 diabetes: etiology, immunology, and therapeutic strategies. Physiol Rev. 2011 Jan;91(1):79-118.
http://www.ncbi.nlm.nih.gov/pubmed/21248163