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Altered expression of CD39 on memory regulatory T cells in type 1 diabetes patients.
Journal of Diabetes 2018 October 15
BACKGROUND: Type 1 diabetes (T1D) is an autoimmune disease, which is the result of autoreactive T lymphocytes attack against pancreatic islet β cells. In recent studies, regulatory T cells (Tregs) have been implicated as being part of the process in T1D. CD39 involved in suppression of inflammation, has been shown to be expressed on Tregs. However, the pathological importance of CD39 to memory Tregs population remains unclear.
METHODS: We investigate subsets of Tregs with a focus on resting, effector and memory Tregs, and CD39 expression in Tregs were detected. Then we examine changes of Treg subsets and Tregs-associated cytokine secretion after CD3/CD28 stimulation of peripheral blood mononuclear cells of diabetic patients and healthy controls. Suppression function of Tregs was measured in mix lymphocyte reaction (MLR).
RESULTS: Our data showed that in T1D patients, Tregs contained a higher percentage of memory Tregs than healthy controls. However, Tregs in T1D patients showed impaired suppression with the low level of Foxp3 expression and low serum IL-10 level. Furthermore, CD39 expression on Tregs was lower in T1D patients than in healthy controls, as well as CD39 expression on memory Tregs. Although the percentage of resting Tregs reduced and effector/memory Tregs increased significantly both in healthy controls and T1D patients after stimulation, CD39 expression on effector/memory Tregs was still reduced in T1D patients with no increase of IL-10 secretion in T1D patients.
CONCLUSION: A defective suppressive function of Tregs in T1D patients was due to a lower expression of CD39 on memory Tregs.
METHODS: We investigate subsets of Tregs with a focus on resting, effector and memory Tregs, and CD39 expression in Tregs were detected. Then we examine changes of Treg subsets and Tregs-associated cytokine secretion after CD3/CD28 stimulation of peripheral blood mononuclear cells of diabetic patients and healthy controls. Suppression function of Tregs was measured in mix lymphocyte reaction (MLR).
RESULTS: Our data showed that in T1D patients, Tregs contained a higher percentage of memory Tregs than healthy controls. However, Tregs in T1D patients showed impaired suppression with the low level of Foxp3 expression and low serum IL-10 level. Furthermore, CD39 expression on Tregs was lower in T1D patients than in healthy controls, as well as CD39 expression on memory Tregs. Although the percentage of resting Tregs reduced and effector/memory Tregs increased significantly both in healthy controls and T1D patients after stimulation, CD39 expression on effector/memory Tregs was still reduced in T1D patients with no increase of IL-10 secretion in T1D patients.
CONCLUSION: A defective suppressive function of Tregs in T1D patients was due to a lower expression of CD39 on memory Tregs.
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