CD39 and diabetes
Children diagnosed with type 1 diabetes (T1D) show signs of low
CD39+/CD45RA+ Treg cells, which may
indicate loss of its suppressive function [166].
Lower expression of CD39 in memory Tregs has been reported as a
potential mechanism explaining the defective suppressive function of
Tregs in T1D patients [167]. The percentages of
CD39+ and
CD39+CD19+ cells were associated
with glycated hemoglobin and fasting plasma glucose levels.
CD39+ cells might have a balancing regulatory role in
the inflammatory process observed in patients with type 2 diabetes (T2D)[168]. The T2D patients with obesity showed
significantly lower percentages of CD39+ Treg cells
and a negative correlation between CD39+ Treg cells
and weight, and body mass index was detected[169]. Mesenchymal stem cells from human gingiva
can migrate to the pancreas and local lymph nodes and act through the
CD39/CD73 pathway to regulate effector T-cells. Infusion of GMSCs
significantly controlled blood glucose levels, delayed diabetes onset,
and ameliorated pathology scores in pancreas[170]. CD39 KO mice developed diabetes more
rapidly and with higher frequency than WT mice, while CD39
overexpressing mice were protected. Furthermore, adoptive transfer
experiments indicated that tissue-restricted overexpression of CD39
conferred robust protection, suggesting that this may be a useful
strategy to protect islet grafts from T cell-mediated injury[171].