. The aim of this study was to investigate the changes of regulatory T cells (Treg), interleukin-6 (IL-6), IL-10, transforming growth factor- (TGF-), and tumor necrosis factor-alpha (TNF-) in patients with type 2 diabetes mellitus (T2DM). . We performed a comprehensive search up to July 2016 for all clinical studies about the changes of Treg, IL-6, IL-10, IL-17, TGF-, and TNF- in T2DM patients versus healthy controls. . A total of 91 articles (5642 cases and 7378 controls) were included for this meta-analysis. Compared with the controls (all < 0.001), the patients had increased serum levels of IL-6, TGF-, and TNF- but decreased the percentage of peripheral CD4CD25Foxp3Treg and serum IL-10 level. Furthermore, the percentage of peripheral CD4CD25Foxp3Treg ( < 0.001) and serum IL-10 level ( = 0.033) were significantly lower in the patients with complication and in the patients without complication, respectively. No significant changes about the percentage of CD4CD25Treg ( = 0.360) and serum IL-17 level ( = 0.459) were found in T2DM patients. . T2DM patients have decreased the percentage of peripheral CD4CD25Foxp3Treg and levels of serum IL-10 but elevated serum levels of IL-6, TGF-, and TNF-. Presence of diabetic complications further lowers the peripheral CD4CD25Foxp3Treg number.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5061980 | PMC |
http://dx.doi.org/10.1155/2016/3694957 | DOI Listing |
Background: Studies have shown that CD4CD25Foxp3Treg cells suppress NKG2D expression on NK cells via a cell contact-dependent mechanism and increased TGF-β and IL-10 production in some cancer models. We herein aimed to explore whether CD4CD25Foxp3Tregs suppress NKG2D-mediated NK cell cytotoxicity in peripheral blood and elucidate the exact mechanism underlying this phenomenon.
Methods: To explore the function of NKG2D, NK cell cultures were treated with an NKG2D-blocking antibody to block these receptors.
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